StemCell Therapy

Toshio Ando is internationally recognized for the development and invention of the in-liquid high-speed atomic force microscope (HS-AFM) for visualizing the dynamics of protein molecules in liquid environments [1-6]. The publication of his seminal paper on HS-AFM in 2008 led Ando and his colleagues to develop derivatives of this technology including non-invasive high-speed scanning ion-conductance microscopy (HS-SICM). "It is a great honor for me to receive this HFSP grant in the worldwide competition," says Professor Ando.

Comments from the HFSP highlighted the strengths of the team and multidisciplinary nature of the proposal, stating: "This is a very strong team of investigators. Each is highly accomplished in their field and brings unique expertise."

Roles of the members of the team:

The Human Frontier Science Program (HFSP) promotes international collaborative basic research on "the elucidation of the sophisticated and complex mechanisms of living organisms". The programs are implemented by the International Human Frontier Science Program Organization (HFSPO) that is based in Strasburg and receives financial support from the governments or research councils of the European Union, Australia, Canada, France, Germany, India, Italy, Japan, Republic of Korea, New Zealand, Norway, Singapore, Switzerland, United Kingdom, and USA.

Selection of references on research published by Professor Ando on high speed AFM

Prof. Toshio Ando

Prof. Toshio Ando

Further general information

About the Human Frontier Science Program2020 awards for Research Grants https://www.hfsp.org/awardees/newly-awarded

About WPI nanoLSI Kanazawa University

Hiroe YonedaVice Director of Public AffairsWPI Nano Life Science Institute (WPI-NanoLSI)Kanazawa UniversityKakuma-machi, Kanazawa 920-1192, JapanEmail: nanolsi-office@adm.kanazawa-u.ac.jpTel: +81(76)234-4550

About Nano Life Science Institute (WPI-NanoLSI)

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Nano Life Science Institute (NanoLSI), Kanazawa University is a research center established in 2017 as part of the World Premier International Research Center Initiative of the Ministry of Education, Culture, Sports, Science and Technology. The objective of this initiative is to form world-tier research centers. NanoLSI combines the foremost knowledge of bio-scanning probe microscopy to establish 'nano-endoscopic techniques' to directly image, analyze, and manipulate biomolecules for insights into mechanisms governing life phenomena such as diseases.

About Kanazawa University

http://www.kanazawa-u.ac.jp/e/

As the leading comprehensive university on the Sea of Japan coast, Kanazawa University has contributed greatly to higher education and academic research in Japan since it was founded in 1949. The University has three colleges and 17 schools offering courses in subjects that include medicine, computer engineering, and humanities.

The University is located on the coast of the Sea of Japan in Kanazawa a city rich in history and culture. The city of Kanazawa has a highly respected intellectual profile since the time of the fiefdom (1598-1867). Kanazawa University is divided into two main campuses: Kakuma and Takaramachi for its approximately 10,200 students including 600 from overseas.

Photo: https://mma.prnewswire.com/media/1142295/Kanazawa_University.jpg

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Toshio Ando of the WPI Nano Life Science Institute, Kanazawa University and Colleagues From Greece, Germany, and USA Have Been Awarded The Prestigious...

Metastatic brain tumor and primary lung cancer were found to have gotten different genetic characteristics in the course of genetic mutation, researchers said.

By making the most of these characteristics, medical professionals will be able to upgrade the effect of targeted therapies, they added

The joint research team of Seoul National University Hospital (SNUH) and Massachusetts General Hospital (MGH) attached to Harvard University College of Medicine has recently released the results of analyzing the genetic mutations of metastatic brain tumors and primary lung cancer.

Brain tumors spread from lung cancer are very malignant, and the number of patients has been increasing recently. However, their treatments have been limited due to their insufficient study

The research team has selected 73 patients suffering from brain tumors spread from lung cancer and analyzed the genetic mutations of metastatic brain tumors and primary lung cancer.

The Korean and U.S. researchers confirmed MYC, YAP1, MMP13, and CDKN2A/B genetic mutations occur in metastatic brain tumors, unlike primary lung cancer. Even the same cancer cells showed different genetic mutations, depending on whether they belong to the lung or brain.

The research team explained this is a very significant finding in the targeted treatment of brain tumors spread from lung cancer. If medical professionals treat patients with targeted therapies developed to suit the characteristics unique to a metastatic brain tumor, they will be able to upgrade therapeutic effects, it added.

The latest research is the result of the seven years of joint study since 2013 between SNUH and MGH. The two institutions have shared case reports and treatment methods through 14 video conferences, and have several joint studies underway by strengthening their cooperation in research.

We jointly published the genetic mutations observed only in metastatic brain tumor in the journal Cancer Discovery jointly with MGH in 2015, said Professor Baek Seon-ha of the Department of Neurosurgery at SNUH. The recent research is its follow-up study, a result of the close cooperation and continuous joint study between the two hospitals.

Professor Park Seong-hye of the Department of Pathology at SNUH also said, This research will exert a decisive influence on the research and deciding on the treatment method of brain tumor spread from lung cancer.

Co-researchers from the U.S. side were Professor Priscilla Brastianos, and research fellow Scott Carter of the Dana-Farber Cancer Institute.

The research results were published on the online edition of the March issue of the journal Nature Genetics.

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New horizon opens for targeted therapy of metastatic brain tumor - Korea Biomedical Review

Buried in the genetic code of the new coronavirus, SARS-CoV-2, which causes COVID-19, are mutations that can help scientists learn more about where the disease started and how its continuing to spread.

Virginias state laboratory is one of three public health labs in the country to begin unraveling that code, Gov. Ralph Northam announced at a news briefing on Monday.

In coordination with the Centers for Disease Control and Prevention and international health partners, the states Division of Consolidated Laboratory Services will begin sequencing virus samples from patients across the commonwealth. By compiling a repository of genetic information, health officials hope to learn more about how the disease began circulating in different communities and whether certain mutations are associated with outbreaks.

Were sequencing the entire genome of the virus, DCLS Director Denise Toney said Monday. We want to determine what are the similarities and what are the differences between what Virginia has and what theyre seeing in European countries, for example, versus southeast Asia versus Washington state.

The technology, often called next-generation sequencing, has actually been around for more than a decade, said Dr. Paul Skolnik, an infectious disease expert and chair of medicine at the Virginia Tech Carilion School of Medicine. Its been used extensively to sequence the genetic code of other infectious diseases, especially HIV.

But unlike HIV which mutates rapidly and can even circulate in individual patients as swarms of closely related viruses SARS-CoV-2 appears to be changing much more slowly. Both Skolnik and Toney said its too early to classify different strains of the disease, and still unclear whether it will ever have that level of variability.

A transmission electron microscopic image from the first U.S. case of COVID-19. The spherical viral particles, colorized blue, contain cross-sections through the viral genome, seen as black dots. (CDC Public Health Image Library)

Usually, there has to be a certain percentage of difference between the sequences to allow us to call something more than one strain, Skolnik said.

He cautioned that more research has to be done before scientists can determine how much variability exists within the virus. But based on the behavior of other coronaviruses, he said its unlikely that SARS-CoV-2 will change fast enough, or extensively enough, to be broken into multiple strains.

What scientists have seen are divergent clusters of the disease, Toney said. So far, there have been roughly seven similar mutations recorded around the world in countries with widespread transmission.

By sequencing samples from COVID-19 patients from Virginia and comparing them with other variants, state health officials have already learned that the disease entered the commonwealth through multiple sources (rather than being spread through exposures to a single patient). Toney said local samples matched with versions from southeast Asia and Europe, as well as other areas of the United States.

Comparing viral sequences can help experts determine which mutations are responsible for outbreaks and which seem to respond to containment measures, she added. It could also help epidemiologists track the disease within communities, determining whether it was introduced by different sources or whether a single version was widely transmitted.

It can give us clues to whether two nursing homes are linked, for example, Toney said. If the strain types are very, very similar and clustered together, it suggests they may have a similar mode of transmission.

From a global perspective, sequencing a wide variety of COVID-19 samples is a valuable tool in developing new treatments and vaccines, Skolnik said. Identifying mutations in the virus allows scientists to determine commonalities between different variants. Knowing which targets are shared in samples around the world will allow researchers to develop drugs that are most effective in interfering with its replication.

Then, it will give us great insight into what made this particular coronavirus so lethal, he added. In that we can understand, from the genetic sequence, what proteins are made and how those proteins differ from coronaviruses that have circulated for eons in the human population. Theres something particular that this particular coronavirus had that made it able to destroy and attack tissue in the lungs.

So far, the state lab has only sequenced a few samples of the virus, Toney said. DCLS is currently working with the Virginia Department of Health to identify which samples would yield the most information through sequencing.

If they have no idea how you got exposed, that could make you a good person to sequence, she added. Maybe it turns out your virus is linked to, say, the Nile River cruises. Then that could link to a nursing home outbreak, or maybe some clusters were seeing in the Northern Virginia area. It can help point to where your exposure may have been.

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Virginia's state lab is one of the first in the country to sequence samples of virus that causes COVID-19 - starexponent.com

A new, different type of coronavirus test is coming that will help significantly in the fight to quell the COVID-19 pandemic, doctors and scientists say.

The first so-called serology test, which detects antibodies to the virus rather than the virus itself, was given emergency approval Thursday by the U.S. Food and Drug Administration. And several more are nearly ready, said Dr. Elizabeth McNally, director of the Northwestern University Feinberg School of Medicine Center for Genetic Medicine.

Youll see many of these roll out in the next couple of weeks, and its great, and it will really help a lot, said McNally, noting doctors and scientists will be able to use it to determine just how widespread the disease is, who can safely return to work and possibly how to develop new treatments for those who are ill.

The serology test involves taking a blood sample and determining if it contains the antibodies that fight the virus. A positive result indicates the person had the virus in the past and is currently immune.

That kind of test will be far easier to roll out and use than the complex nasal swab tests now being used to detect the active virus that causes COVID-19, she added, saying its possible that the antibody tests could be conducted in the confines of ones own home, much like a pregnancy test.

They will come in a variety of shapes and sizes, McNally said. "The simplest would be one that you do at home, that you would poke your finger and squeeze out a little blood and put it on a little strip, and itll be the plus-minus whether youve developed antibodies or not.

There are several benefits to having the test, including:

Determining how much of the population is infected.

One of the questions we are going to be asking is, How widespread was this virus? McNally said. "I think we have a lot of indication that its much more widespread than we know, because most of the younger people who get this get it relatively mildly, recover and do OK. And were not tracking any of those people right now.

Interestingly, the more people who have had it, the safer everyone is, under the concept of herd immunity.

The people who are already covered can actually provide protection to the people around them, just because its hard for the virus to spread, McNally said. The virus cant spread anymore, so people are less likely to get it.

Figuring out who can go back to work, particularly sidelined doctors and nurses, police officers and firefighters.

If a person is positive for antibodies, which likely show up two to six weeks after infection, theyre not going to get sick or spread the virus, because their bodies are killing it off. Once the antibodies come up in your system, that means your body fought it off, and you dont have active virus, McNally said.

It may also be important to test grocery store workers, McNally added, noting that buying food is one of the things thats still forcing people out of their homes. Thats one of the major points of contact, so where we can reduce that, especially in the next few weeks, I think thats going to be really critical, she said.

Getting a sense of how long immunity lasts.

Other coronaviruses that have been studied trigger antibodies that typically last one to three years. So the immunity likely isnt forever.

Are we seeing a sustained response thats going to help us prepare better for when this happens again, and it will happen again, McNally said. Thats what happens with viruses.

Possibly learning more about how to fight the disease, using antibody treatment.

Maybe these people that really did poorly (when they had COVID-19), maybe they were slow to develop antibodies, in which case this concept of giving them antibodies is actually a good concept to help treat people, McNally said. "So, theres so many things we will learn from the immune response to this virus.

Approval of the antibody test is something that public health officials have been talking about for weeks, saying it couldnt come fast enough.

When we have antibody testing, trust me, well be using that a lot, because well be looking to see if people have been exposed to coronavirus, Dr. Allison Arwady, Chicagos public health commissioner, said in a recent interview before the test was approved. Are they recovered? Will they be safe for working and caring for people?

Likewise, Dr. Robert Gallo, co-founder and director of the Institute of Human Virology at the University of Maryland School of Medicine, described development of the test as imperative.

It allows the public health officials to better follow the epidemic," Gallo said. "Without the antibody test, its very hard to follow the epidemic with convenience of any kind.

Research wise, wouldnt it be really important to know if theres some aspect of the immune system that makes it worse, or if there are people correlating with some type of immune response that was really correlated with the symptoms being virtually nothing," he added. You would just be able to make really important conclusions, so we need the antibody test rather desperately.

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Next coronavirus test can tell if you are now immune and its fast - Monmouth Daily Review Atlas

SALT LAKE CITY, April 08, 2020 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc. (NASDAQ: MYGN), a global leader in personalized medicine, announced today that due to the impact of the global COVID-19 pandemic, the company is withdrawing its fiscal year 2020 financial guidance.

Prior to mid-March we were experiencing volume trends consistent with our expectations across all products; however, recent social distancing guidelines have had a significant impact on test volume trends in late March and into the fiscal fourth-quarter, said R. Bryan Riggsbee, interim president and CEO and chief financial officer at Myriad Genetics. Our priority as an organization during the coronavirus pandemic has been to maintain business continuity and access to testing, while ensuring the safety of our employees and customers. As an organization we have taken steps to advance these dual aims, and I am very proud of how the Myriad team has responded to the crisis.

In responding to the pandemic, Myriad has made several changes to its business practices to promote the safety of both customers and employees including ceasing in-office sales calls and implementing virtual selling, granting all non-essential personnel the ability to work from home, enabling direct sample collection for patients and implementing policies to improve laboratory personnel safety.

While the uncertain timeframe of the Coronavirus pandemic makes it difficult to predict future business trends for the company, the company will provide an update on its business, including the impact of COVID-19, on its next quarterly earnings call.

About Myriad GeneticsMyriad Genetics, Inc. is a leading personalized medicine company dedicated to being a trusted advisor transforming patient lives worldwide with pioneering molecular diagnostics. Myriad discovers and commercializes molecular diagnostic tests that determine the risk of developing disease, accurately diagnose disease, assess the risk of disease progression, and guide treatment decisions across six major medical specialties where molecular diagnostics can significantly improve patient care and lower healthcare costs. Myriad is focused on three strategic imperatives: transitioning and expanding its hereditary cancer testing markets, diversifying its product portfolio through the introduction of new products and increasing the revenue contribution from international markets. For more information on how Myriad is making a difference, please visit the Company's website: http://www.myriad.com.

Myriad, the Myriad logo, BART, BRACAnalysis, Colaris, Colaris AP, myPath, myRisk, Myriad myRisk, myRisk Hereditary Cancer, myChoice, myPlan, BRACAnalysis CDx, Tumor BRACAnalysis CDx, myChoice HRD, Vectra, Prequel, ForeSight, GeneSight and Prolaris are trademarks or registered trademarks of Myriad Genetics, Inc. or its wholly owned subsidiaries in the United States and foreign countries. MYGN-F, MYGN-G.

Safe Harbor StatementThis press release contains "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995, including statements relating to maintaining the Companys global leadership in precision medicine and the Company's strategic directives under the caption "About Myriad Genetics." These "forward-looking statements" are based on management's present expectations of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those described or implied in the forward-looking statements. These risks include, but are not limited to: the risk that sales and profit margins of the Companys existing molecular diagnostic tests and pharmaceutical and clinical services may decline or will not continue to increase at historical rates; risks related to the Companys ability to successfully transition from its existing product portfolio to our new tests; risks related to changes in the governmental or private insurers reimbursement levels for the Companys tests or the Companys ability to obtain reimbursement for its new tests at comparable levels to its existing tests; risks related to increased competition and the development of new competing tests and services; the risk that the Company may be unable to develop or achieve commercial success for additional molecular diagnostic tests and pharmaceutical and clinical services in a timely manner, or at all; the risk that the Company may not successfully develop new markets for its molecular diagnostic tests and pharmaceutical and clinical services, including the Companys ability to successfully generate revenue outside the United States; the risk that licenses to the technology underlying the Companys molecular diagnostic tests and pharmaceutical and clinical services tests and any future tests are terminated or cannot be maintained on satisfactory terms; risks related to delays or other problems with operating the Companys laboratory testing facilities; risks related to public concern over the Companys genetic testing in general or the Companys tests in particular; risks related to regulatory requirements or enforcement in the United States and foreign countries and changes in the structure of the healthcare system or healthcare payment systems; risks related to the Companys ability to obtain new corporate collaborations or licenses and acquire new technologies or businesses on satisfactory terms, if at all; risks related to the Companys ability to successfully integrate and derive benefits from any technologies or businesses that it licenses or acquires; risks related to the Companys projections about the potential market opportunity for the Companys products; the risk that the Company or its licensors may be unable to protect or that third parties will infringe the proprietary technologies underlying the Companys tests; the risk of patent-infringement claims or challenges to the validity of the Companys patents; risks related to changes in intellectual property laws covering the Companys molecular diagnostic tests and pharmaceutical and clinical services and patents or enforcement in the United States and foreign countries, such as the Supreme Court decisions Mayo Collab. Servs. v. Prometheus Labs., Inc., 566 U.S. 66 (2012), Assn for Molecular Pathology v. Myriad Genetics, Inc., 569 U.S. 576 (2013), and Alice Corp. v. CLS Bank Intl, 573 U.S. 208 (2014); risks of new, changing and competitive technologies and regulations in the United States and internationally; the risk that the Company may be unable to comply with financial operating covenants under the Companys credit or lending agreements; the risk that the Company will be unable to pay, when due, amounts due under the Companys credit or lending agreements; and other factors discussed under the heading "Risk Factors" contained in Item 1A of the Companys most recent Annual Report on Form 10-K filed with the Securities and Exchange Commission, as well as any updates to those risk factors filed from time to time in the Companys Quarterly Reports on Form 10-Q or Current Reports on Form 8-K. All information in this press release is as of the date of the release, and Myriad undertakes no duty to update this information unless required by law.

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Myriad Withdrawing Financial Guidance for FY2020 Due to Business Impact from Coronavirus Pandemic - BioSpace

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A genetic variant in a gene called MET is responsible for more aggressive growth of head and neck cancer, and lung cancer, according to a new study.

A further probe into the finding reveals therapeutic strategies that could potentially target this genetic alteration and pave the way for better and more effective treatments.

The MET gene encodes for a cancer promoting protein that relays growth, survival, and transmission of signals in cancer cells, researchers say.

As reported in Nature Communications, researchers also identified a form of MET protein which showed ethnic preference with higher incidence among Asians, and associated with poorer prognosis in patients diagnosed with head and neck squamous cell carcinoma or lung squamous cell carcinoma.

Even though the MET variant does not seem to predispose someone to head and neck cancer or lung cancer, it leads to more aggressive growth of cancers that have already developed.

Unlike other MET mutants, existing MET-blocking drugs do not seem to inhibit this genetic variant, prompting researchers to conduct further investigation on the mechanism behind the genetic alteration.

The team found that the single amino-acid change in the MET receptor from the genetic alteration leads to preferential strong binding to another cancer promoting protein, HER2. Both proteins then work together to drive cancer aggression and allow the cancer cells to survive therapies that involve MET-blocking drugs.

The mechanism of this MET variant is novel and unreported. This finding contributes to the growing evidence of the role of genetic variants in affecting clinical outcome, and underscores the importance of diving deep into our genetic inheritance in cancer research, says Kong Li Ren of the Cancer Science Institute (CSI) Singapore at NUS, who initiated the study.

Knowledge of this unique mechanism also allowed researchers to identify several HER2 inhibitors capable of blocking cancer progression the genetic alteration caused.

Our study represents a conceptual advancement to cancer research, as we have shown that it is possible to block the activity of a cancer-driving gene by administrating a targeted therapy directed not against the mutant protein in question, but rather, a corresponding protein with which it binds to, says Goh Boon Cher, deputy director and senior principal investigator at CSI Singapore.

The remarkable anti-tumor responses observed in our experimental models, coupled with the availability of FDA-approved HER2 inhibitors, also presents a huge opportunity for clinicians to improve disease outcome of this genetic alteration via precision medicine.

The research team is now translating the findings to a clinical trial where patients tested positive for this MET variant gene are treated with suitable medications that have shown effectiveness in the laboratory.

Additional coauthors are from the National University Cancer Institute, the National Cancer Centre Singapore, and the Bioinformatics Institute at the Agency for Science, Technology and Research, Singapore.

Source: National University of Singapore

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Gene variant makes head and neck cancer more aggressive - Futurity: Research News

This article originally appeared on VICE US.

There was a time when waking up with a scratchy throat or a dry cough didnt elicit such a sense of dread, but Covid-19 has made us all hyper-aware of its symptoms. Many people have been left wondering if they are asymptomatic carriers of the disease, or if a slight cold they may have recently experienced was actually something more menacing.

These fears are not unfounded: More than a million patients around the world have confirmed cases of coronavirus, but the real number of infections is far higherthough nobody yet knows by how much.

Thats why medical professionals are rushing to develop tests for antibodies that might reveal if a patient ever contracted Covid-19, regardless of whether they experienced symptoms. These tests may even be able to determine individual immunities to the virus, which has led to speculation that some people could reenter the workforce or resume normal activities if they have the right antibodies.

While this proposed solution may provide a sense of hope, it is far from a certain outcome at this point in time. Theres no clear consensus about the immunological response to Covid-19, and murky ethical problems undergird the idea of lifting restrictions on some populations, while isolating others, especially based on unsettled science.

Heres what you need to know about these tests, their development, and their potential to influence the global Covid-19 response.

Antibody tests, also known as serological tests, differ from the diagnostic swab tests that have been in high demand since the pandemic gained momentum.

Swab tests, or PCR tests, are designed to directly detect the virus by searching for its RNA, which is a genetic signature of its presence. These tests require collection of mucus samples from patients, typically sourced from deep within the nasal cavity, which are then sent to a laboratory to be examined. If the results come back positive, the patient is considered an active carrier of Covid-19 who could potentially infect other people.

Antibody tests, in contrast, dont look for the virus itself, but rather our immunological response to it. When our bodies are invaded by antigens such as the coronavirus, our immune systems react by creating a type of blood protein called an antibody. Antibodies flow through the blood, attacking the alien antigens by binding to them, which can neutralize the spread of infection. Many known antibodies can be detected with a quick blood test.

The idea is that you have volunteers who have recovered from infection, and you look to see what antibodies theyre expressing and test that against samples of the virus, basically, to see what are the circulating antibodies that recognize your virus, said Ruth Collins, professor of molecular medicine at Cornell University College of Veterinary Medicine, in a call.

It can take several weeks for the immune system to develop antibodies to fight a virus, which means positive serological tests may not indicate an active infection. Instead, the presence of coronavirus antibodies demonstrates if a patient ever had Covid-19, whether or not they experienced symptoms.

While it is common for an exposed person to develop immunity to other known viruses, it is important to emphasize that nobody knows yet whether the presence of Covid-19 antibodies indicates that a patient has either temporary or permanent immunity to the infection.

We dont know yet exactly how peoples immune systems respond to the infection, so wed have to find something that would mark everybodys response to the virusthe universal human response to the virusand to make sure that it was specific to this virus, Collins said.

These things are doable, she added, they just take a long time to work out.

Short answer: We have no idea.

Countless teams of scientists around the world are developing serological tests to detect antibodies related to Covid-19, including researchers at the Centers for Disease Control (CDC). Last Thursday, the US Food and Drug Administration approved the first test for antibodies test for Covid-19, though it is intended as a diagnostic test for active infections.

Last week, a team of scientists at Stanford University conducted finger-prick blood tests on 3,200 volunteers to help refine their antibody test. Likewise, in Italy, an entire town of 3,000 people that already received swab tests is now in the process of providing blood samples to follow-up on the diagnostic data with antibody studies.

Regardless, there have also been setbacks with the roughly 100 test kits for these antibodies that are already in development. None of these tests are close to reaching the high bar required for public distribution.

"Theres so much we really dont know"

Youd have to have a very high specificity and sensitivity, so you would be able to pick up even small amounts of those antibodies or the evidence of infection in people's blood, Collins said. Without that, you could well have people that have been infected without knowing about it, she continued, or people who might think they were still naive, immunologically, when in fact they werent.

In other words, antibody tests not only need to be good enough to yield reliable positive results, they also need to clearly show who does not have Covid-19 antibodies. Finding the right balance requires making sure that antibodies linked to viruses that arent Covid-19 do not produce false positives, and ensuring that the antibodies that are specifically linked to this particular coronavirus cannot evade detection.

Its hard to predict how long this process will take, given that so many teams are actively working on it, but its probably optimistic to expect they will take weeks or even months to be widely available to the public.

This timeline might be further delayed by new revelations about Covid-19. For instance, its possible that some carriers may never develop symptoms, but could still remain infectious to others for months.

Theres not even a consensus that everybody will completely clear the virus from their system, Collins noted. Some people may be asymptomatic shedders for a while. Theres so much we really dont know.

The phrase immunity passport has been floated by the government of the United Kingdom, and others, as a potential way to allow people with immunity to Covid-19 to return to regular work and travel routines.

Assuming that widespread serological testing is achievable, the idea is that people with antibodies linked to Covid-19 would be cleared of social distancing measures because they are theoretically immune to the virus and cannot actively spread it. This would bring back some normalcy for some of the population, and it would also enable scientists to better estimate the total number of Covid-19 cases, as opposed to confirmed cases involving patients who were sick enough to receive a swab test.

On the flip side, antibody tests for this purpose raise concerns about privacy rights and employment inequities, given that authorities would be using medical information to judge whether patients can return to work and normal life.

In the United States, the Americans with Disabilities Act (ADA) and the Genetic Information Act (GINA) prevent employers from discriminating on the basis of disability or genetic information. But discrimination for health reasons remains legal in many contexts in the United States, according to Jessica Roberts, director of the Health Law and Policy Institute at the University of Houston Law Center.

"We can go some way towards knowing who has been infected, but the idea of it being used as employment criteria is somewhat dystopian

Both laws would likely permit employers to screen employees for antibodies, Roberts said in an email. She noted that GINA only applies to genetic test results and family medical history, which are not likely to apply to antibody tests, which do not look for individual genetic information.

Moreover, the ADA actually allows employers to discriminate if employing a person with a disability could threaten the safety of the workplace, Roberts added. Assuming that ADA protection applies to people with Covid-19 (which a court would have to ask whether having Covid-19 constitutes a legally recognized disability), the employer could still prohibit an employee from coming to work if the employer could show that the employee would pose a significant risk.

The notion of planning a staggered reopening of society, in which restrictions are lifted on people judged immune to Covid-19, is inherently risky on both an epidemiological and ethical level.

While it may be soothing to daydream about receiving an immunity passport that allows you to return to your "normal" life, it is probably better to invest your energy in adapting to the restrictions, following health guidelines until more information is available, and working towards a better "normal" in whatever way you can.

It sounds good because it gives us what we want, which is definitive answers, Collins said.

But we dont know enough to be able to provide those definitive answers. We can go some way towards knowing who has been infected, but the idea of it being used as employment criteria is somewhat dystopian.

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What Are Antibody Tests, and Can They Prove Coronavirus Immunity? - VICE

Siddhartha Mukherjee and Ken Burns hope The Gene will spark a national conversation. Photo: Stephanie Berger/Columbia University

NEW YORK Surging hope and semblance of solace in the age of the coronavirus comes in what may seem as strange indicators for laymen: New York state registered the largest number of deaths in a single day, on Tuesday, April 7, 2020, from the coronavirus since the crisis began. A staggering number of 731 people died in a day. Yet, there was cautious optimism as the rate of hospitalizations has fallen for several days, and the infections seem to be plateauing.

Gov. Andrew M. Cuomo, while revealing that 5,489 people had died in the state, said he was encouraged by the data on hospitalizations. He, however, cautioned against growing complacent or easing up on social distancing measures that seem to be working, reported The New York Times.

Cuomo said that increases in hospital beds and the number of health care providers who were working had helped New York to balance its patient load and help ensure that no one facility was overburdened.

The governor also said that planning was underway to restart the regional economy and that he had spoken to the governors of New Jersey and Connecticut about coordinating those efforts.

While the news on the lower number of hospitalizations may be encouraging for many, for families who are either victims or afflicted with the coronavirus, there was only misery, despair and dread to deal with.

A veteran Indian American journalist, Brahm Kanchibotla, from Hicksville, NY, was amongst the thousands who have died from the coronavirus, in New York. He breathed his last on April 6, after a cardiac arrest in a hospital in New York, after being admitted following symptoms of coronavirus. He is survived by his wife Anjana, and two children, son Sudama, and daughter Siujana.

Kanchibotla, who had worked for The Indian Express newspaper in Hyderabad, prior to emigrating to the US, worked also for the United News of India, from New York, and had worked as Content Editor for Merger Markets. He was 66 years old, according to Rajender Dichpally, a community activist.

Dichpally expressed his shock at the passing away of Kanchibotla, who he said was put on a ventilator at the hospital in New York, but didnt pull through.

He took his profession very seriously, said Dichpally. I remember when the late YSR Reddy had come to New York, in 2002. Kanchibotla wanted to interview him, and I managed to seat him next to YSR as he was having dinner, and Kanchibotla managed to get the interview.

Dichpally, who is from the Telugu diaspora, said that Kanchibotla also covered several Telugu association meets in the US, annually.

Mohammed Jaffer, the Editor of SnapsIndia, an international news photo service, based also in New Jersey, said that he knew Kanchibotla for the last 30 years, and they both were from the same hometown, Hyderabad.

I knew him for 30 years. He used to work for Indian Express Hyderabad, and he also used to work with my father there. He was a very humble and down to earth man, said Jaffer.

SIDDHARTHA MUKHERJEES NEW VENTURE

Indian American oncologist and writer Siddhartha Mukherjee and Ken Burns will present the PBS Premiere of The Gene: An Intimate History.

The ability to modify genes and prevent disease has exploded in the last decade. It is now possible to use gene therapy to cure inherited disorders, to correct genetic defects and to limit the severity of a disease. But this new era in genomic medicine offers both promise and peril, according to a report by Columbia University, where Mukherjee is on the faculty.

These revolutionary discoveries highlight the awesome responsibility that we have to make wise decisions, not just for the people alive today, but for generations to come, said Mukherjee, an assistant professor of medicine at Columbia University Irving Medical Center, staff cancer physician and author of The Gene: An Intimate History.

The Gene: An Intimate History, a four-hour, two-part documentary, will air April 7 and 14 on PBS stations nationwide. The series, like the book, weaves together science, history and stories of individuals and families, including Mukherjees account of his own family and its recurring pattern of mental illness.

The Gene airs at a critical moment for the science community, as geneticists around the world grapple with the ethical questions these technologies raise. In Nov. 2018, a Chinese researcher stunned and horrified the scientific community with the announcement that he had created the first genetically edited babies, twin girls born in China.

The documentary had been cut and finished just before the first cases of coronavirus were reported in China, so it was too late to include what would soon become the COVID-19 pandemic, a global crisis inextricably tied to our genes, Mukherjee said, reported Columbia University.

A piece of genetic material29,000-odd nucleotides of RNAcoated with protein has upended the world, Mukherjee said. Virtually every technology were using to track and treat COVID-19, even an oral or nasal swab to detect whether you are infected, relies on genetic techniques.

In an interview to Columbia News, Mukherjee sad that perhaps the most grotesque example of the misuse of the language of genetics is the Nazi eugenics program in the 1930s. The Nazis distorted the language of genes to imagine creating a genetically superior nationand then this was used to justify imprisonment and mass extermination.

Mukherjee was asked that if the concept of being able to order for $200 a profile of his or her genome that provides ancestral information, as well as genetic health risks, was positive or not.

He responded: The question you have to ask is do we want to live in a world where you can send a sample of saliva and find out that you have a 10 percent or 20 percent risk of developing breast cancer in the next 30 years. This information can be useful, motivating you to adopt more positive health behaviors. But it also marks you, changes you. It can change your relationship with yourself, your body. When you decide to test for future risk you are also, inevitably, asking yourself, what kind of future am I willing to risk?

Asked if genetics play a role in how vulnerable a person is to contracting COVID-19, and whether that person is more at risk of dying from the illness, he said this is one of the great mysteries of this infection. Young, healthy people are dying, even if most serious cases occur in the elderly and those with pre-existing conditions.

Mukherjee added: There are multiple studies trying to unravel why some people infected with SARS-Cov2, the virus that causes COVID-19, fall seriously ill, while others show only mild or nonexistent symptoms. We are finding a correlation between high viral loadthe amount of virus present in any sample taken from a patientand more severe illness.

Mukherjee had recently argued in The New Yorker that we have done a good job measuring the spread of the virus across populations, but it is now time we learn more about how SARS-Cov2 behaves in the body. This requires large-scale efforts to collect the DNA of people and the virus that they are infected with. One example of a study might be taking the DNA of those with serious underlying disease and comparing it to the DNA of those with mild or asymptomatic cases.

According to him, the medical fraternity need to determine whether genetic variations among humans affect how susceptible individuals are to COVID-19 infections as rapidly as possible.

(Sujeet Rajan is Executive Editor, Parikh Worldwide Media. Email him: sujeet@newsindiatimes.com Follow him on Twitter @SujeetRajan1)

Read more:
Death of a journalist, and Siddhartha Mukherjee on genes and COVID-19 - newsindiatimes.com

The COVID-19 pandemic is piling on top of a litany of health inequalities in America to kill a disproportionate number of African Americans. In Chicago alone, black residents make up more than half of all cases and about 70 percent of those whove died of the disease. Thats despite African Americans only making up about 30 percent of the citys population.

Those numbers take your breath away, they really do, Chicago mayor Lori Lightfoot said in response at a press conference on April 6th. This is a call-to-action moment for all of us.

Experts who have long grappled with higher rates of chronic conditions like diabetes, heart disease, and asthma in black communities arent surprised. The barriers and biases that laid the groundwork for African Americans to be potentially harder hit in this crisis have been in place for generations, they say. Ensuring better health outcomes in this pandemic or any future public health crisis means addressing those underlying injustices.

When you look at [COVID-19] that particularly is virulent for persons who have higher rates of disease, thats exactly the picture of African Americans. But its not their genes. Its the social conditions that we have created, says, David Williams, a professor of public health at Harvard whose research has examined how race and class affect health. I hope this is a wake up call for America.

Its hard to get a grasp on how discriminating the spread of the disease in the US really is; limited testing nationwide means we dont even have a good baseline for how many Americans have contracted COVID-19. Many states arent reporting the breakdown of their cases by race, and many localities disclosing the race of COVID-19 patients dont have demographic data for every single case. The data that we do have, however, is beginning to show a stark divide across the nation.

In Michigan, African Americans make up a third of all cases and 40 percent of deaths, while making up just 14 percent of the states population. And 70 percent of people whove died of COVID-19 in Louisiana as of April 6th were African American; less than one-third of the states population is black. In Alabama, an equal number of black and white residents have died, but 69 percent of the population is white while roughly 27 percent is black.

I have seen in my waiting room mostly black and brown patients who are essential workers and service workers who cant afford to stay home. These are the ones that I see presenting to the clinic with COVID-19 symptoms, said Uch Blackstock, a physician in Brooklyn and CEO of the company Advancing Health Equity, in an April 6th press call.

On April 8th, New York the state that has more than a third of all the cases in the US released data on race for the first time, backing up Blackstocks earlier observations. Black New Yorkers made up 18 percent of deaths to COVID-19 in the state (outside of New York City), although theyre just 9 percent of the population. In the Big Apple, Hispanic and black people have died at rates 5 to 6 percent higher than the percentage of the population they make up.

The disparities that have plagued this city, this nation, that are all about fundamental inequality are once again causing such pain and causing innocent people to lose their lives, New York City Mayor Bill de Blasio said in a press conference today. Its sick. Its troubling. Its wrong.

Improving the odds for neighborhoods of color, Williams says, will mean addressing the cascade of disparities when it comes to housing, air quality, education, and job opportunities. Your zip code is a better predictor of how long and how well you will live than your genetic code, Williams says.

Chicago has the biggest differences in life expectancies based on ZIP code in the US, according to data from NYU Langone Health. There, the neighborhood with the lowest life expectancy 60 years has a population thats almost 95 percent black. Meanwhile, the neighborhood with the highest life expectancy 90 years is predominantly white.

Without closing those neighborhood-to-neighborhood gaps, Williams fears that the economic fallout from COVID-19 could make health disparities even worse in the future. Without that investment, I shudder to think of what the long term effects are going to be, he says.

COVID-19 is deadlier in people who have preexisting health conditions that weaken their lungs and immune systems. Black Americans were already three times more likely to die from asthma-related causes in 2014, according to the US Department of Health and Human Services. Living in neighborhoods with more air pollution is likely a contributing factor: African Americans were 75 percent more likely to live in places bordering a polluting facility like a factory or refinery compared to other Americans, according to a 2017 report by the NAACP and Clean Air Task Force. Theyre also exposed to air thats 38 percent more polluted in comparison to white Americans, the report found.

Heightened risks for African Americans are paired with lower rates of being insured and lower median household incomes in comparison to whites, which can limit access to health care. Williams also points out that black households are less likely to have an economic cushion to help them get through the pandemic and its aftermath since they have 10 cents in wealth for every dollar that white households have accumulated.

While anyone struggling to make ends meet is especially vulnerable right now, Williams points out that people of color face the added burdens of racism and discrimination when trying to get medical care. Racial and ethnic minorities tend to get worse care compared to whites, regardless of insurance status, income, age, or severity of conditions, a comprehensive 2003 report from the National Academies Institute of Medicine found. Across virtually every therapeutic intervention, from the most simple medical procedure to the most complicated, blacks and other minorities receive poorer quality care and less intensive care than whites, Williams says. He fears the same could be playing out now.

Theres already some early evidence that testing for COVID-19 might have been out of reach for many African Americans, which could lead to a silent spread of the disease among black communities, says Syracuse University associate professor Shannon Monnat. States with more black residents and higher poverty rates had lower rates of testing for COVID-19, according to preliminary data published by Syracuse University last week. Those early figures similarly suffer from a poor baseline since testing has been low across the board for all Americans. But Monnat says that places that have large concentrations of vulnerable populations, including racial and ethnic minorities and poorer residents, tend to have poorer health care infrastructure, which could lead to less access to COVID-19 tests.

In response to New Yorks newly released numbers, Gov. Andrew Cuomo said that the state would increase its testing in minority communities and conduct research on why the state is seeing those gaps. Thats a late start considering the state has seen an exponential growth in cases for weeks, but it could serve as a lesson for other big cities bracing for a surge of infections.

You can almost predict with certainty that already marginalized and vulnerable populations will be getting tested less frequently and less easily than other populations, says Irwin Redlener, director of the National Center for Disaster Preparedness at Columbia University. They are always at risk for not getting whats needed, especially and including in times of disaster.

Read more from the original source:
America set up black communities to be harder hit by COVID-19 - The Verge

Public health officials have been warning that a Covid-19 vaccine will not be available to the public for 12 to 18 months, dampening hopes that there will be a quick end to the global pandemic nightmare.

But Chinese researchers cracked the virus' genetic code within weeks of its emergence late last year, and two vaccine candidates are already in early human trials one in China and the other in the United States.

What's the hold up?

Essentially, you can speed up the vaccine development process to respond to a pandemic, but you don't want to speed it up so much that you allow a bad vaccine to enter the market, explained Dr Greg Poland, director of the Mayo Clinic's Vaccine Research Group.

"The process of developing, testing and licencing a vaccine for widespread population use is designed to be slow, deliberative, peer-reviewed, reflective, evidence-based, so that we don't make mistakes," Poland said.

Going too fast could lead to a vaccine that's not effective or, worse, can cause serious health problems, Poland said.

Typically, clinical trials take 10 to 15 years and a billion dollars to complete, Poland said.

Vaccine trials come in three phases, said Dr Wilbur Chen, an adult infectious disease expert at the University of Maryland's Center for Vaccine Development and Global Health:

The US vaccine candidate now in clinical trials was developed at record speed by scientists at the US National Institute of Allergy and Infectious Diseases (NIAID) and the biotech company Moderna.

"This was very dramatic that we were able to have the first Covid-19 vaccine into clinical trials within just a couple of months," Chen noted.

Researchers combined the virus' genetic code with existing processes to create the vaccine candidate, said Dr Kathleen Neuzil, director of the University of Maryland's Center for Vaccine Development and Global Health, in Baltimore.

"The reason we were able to get into trials so quickly is because this vaccine was modelled on other vaccines for influenza and Zika, using the same manufacturing process and the same technology, but just substituting the genetic code for this SARS-CoV2 virus," Neuzil said.

This trial has enlisted 45 healthy adults in Seattle, who are being tracked for about six weeks.

The Covid-19 virus infects lung cells using "spike" proteins that line the outside of the virus. These spikes bump into receptors on the lung cells, tricking the cells into letting the virus enter and infect them.

The NIAID/Moderna vaccine aims to teach the immune system to recognise these spike proteins and destroy the virus.

The US Food and Drug Administration has indicated that it is willing to speed up the regulatory process by allowing clinical trial phases to be combined.

For example, phase I and II trials could be combined by tracking both safety and immune response. Phase II trial participants could be followed into phase III, and tracked to see if the vaccine prevents community infection.

"We know we are in the middle of a pandemic right now, so we are very carefully following safety, but we really can't forget we're now at about the million mark for people infected with Covid-19," Neuzil said.

But Poland warned there are potential pitfalls that need to be considered in rushing a vaccine to market.

For example, the vaccine might not provide lasting immunity, either because people's immunity wanes quickly or because the virus mutates to get around it.

There already are concerns regarding the ability of people to remain immune to coronaviruses. People typically lose their immunity to coronavirus strains that cause the common cold within a year, Chen said.

Poland also is concerned about the focus of the NIAID/Moderna vaccine and other similar candidates on the "spike" or "S" protein alone.

"That's one area where there's been at least one identified mutation," Poland said of the coronavirus spike protein. "You put a mutational pressure on an RNA virus and, no surprise, the virus mutates and changes."

By comparison, flu vaccines include antigens related to two separate proteins on the influenza virus, to limit the virus' ability to mutate away from a person's established immunity, Poland explained.

Another concern is the potential for unintended safety consequences related to the vaccine.

"Something rushed out too fast that would have some significant side effect later would set back vaccine acceptance in an already vaccine-sceptical culture for decades," Poland said.

Neuzil noted that "when we have seen safety signals with vaccines, they ordinarily occur soon after you give the vaccine".

However, vaccine candidates earlier developed for the coronaviruses behind SARS (severe acute respiratory syndrome) and MERS (Middle East respiratory syndrome) have raised concerns about creating lung disease on their own, according to a recent editorial in the New England Journal of Medicine.

The SARS vaccine candidates tended to cause "antibody-enhanced disease" in animal testing, a condition in which a creature that's received a vaccine not only gets infected by the target virus but also suffers worse symptoms than if they'd never been inoculated, Poland explained.

"It protected them from the virus, at the cost of antibody-enhanced disease. These animals developed an unusual immunopathological picture in their lungs and livers. The vaccines never progressed past that," Poland said.

Similar antibody-enhanced disease reactions also occurred in the 1960s with an inactivated measles vaccine and in 2018 with a vaccine for dengue, Poland said.

Poland foresees a potential future in which a Covid-19 vaccine is rushed out but proves ineffective in preventing infection, possibly because the virus has mutated around the vaccine. "A second strain develops next year that, when it infects people who have been immunised, they are not protected because of the false immunity they have or develop antibody-enhanced disease," he said.

There are as many as 40 vaccine candidates for Covid-19 in various stages of development, Poland said.

A second US company, Inovio Pharmaceuticals, announced on Monday that it is beginning phase I clinical trials in 40 healthy volunteers in Philadelphia and Kansas City, Missouri. This vaccine uses a section of the virus' genetic code packaged inside a piece of synthetic DNA.

Having many vaccine candidates will help in the process of speeding a successful vaccine to the public, Neuzil said.

"You can't count on a single vaccine," Neuzil said. "We want a lot of shots on goal right now, hoping that we'll score with at least one of these."

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Image credit: National Cancer Institute, Unsplash

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Why will it take so long for a Covid-19 vaccine? - Health24

Investigators have identified genomic alterations that appear to be associated with prognosis in men with metastatic castration-sensitive prostate cancer (mCSPC).

Astudy of 424 patients with mCSPC treated at a tertiary care center revealedthat alterations in the androgen receptor (AR), TP53, cell-cycle, MYC oncogenicsignaling pathways occur more commonly in tumors with worse overall survivaland decreased time to castration-resistant disease, whereas alterations in theSPOP and MNT pathways occur more frequently in tumors with a better prognosis,according to findings published in ClinicalCancer Research.

Thegenomics of metastatic castration-sensitive prostate cancer have not been wellcharacterized in the literature, but it is now clear that upfront treatmentintensification with taxanes or next-generation AR-directed therapies offerbenefit in the overall patient population, said the studys co-senior authorWassim Abida, MD, a medical oncologist at Memorial Sloan Kettering CancerCenter in New York. The question remains whether treatment selection ortargeted therapies can be employed based on genomic characteristics.

Theassociation between alterations in cell-cycle genes and TP53 and MYC pathwaygenes and worse outcomes may pave the way for targeted therapy in thesehigher-risk groups, Dr Abida said.

Thestudy compared genomic alterations according to clinical phenotypes: high- vslow-volume disease and de novo vsmetastatic recurrence. Of the 424 patients in the study, 213 men (50%) hadhigh-volume disease (4 or more bone metastases or visceral metastases) and 211(50%) had low-volume disease; 65% had de novometastases and 35% had metastatic recurrence. At the time of sample collection, patients had a medianage of 66 years. The investigators conducted gene sequencing from May 2015 to September2018.

High- vs low-volume disease

Inadjusted analyses, men with higher-volume disease had significant 1.8- and3.7-fold increased risks of castration-resistant disease and death,respectively, compared with men who had low-volume disease. Tumor specimensfrom men with high-volume disease had more copy number alterations.

Amongmen with high-volume disease, the highest-ranking pathways were the NOTCH,cell-cycle, and epigenetic modifiers pathways.

Althoughthe prevalence of CDK12 alterations differed between patients with de novo metastatic and those with metastaticrecurrences, the groups had similar prognoses. I was actually surprised therewere not more dramatic genomic differences between de novo and relapsed disease, said study co-senior author PhilipKantoff, MD, a medical oncologist and Chair of the Department of Medicine atMemorial Sloan Kettering Cancer Center in New York.

Afteradjusting for disease volume and other genomic pathways, the researchers foundthat the rates of castration resistance differed by 1.5-fold and up to 5-fold accordingto alterations in the AR, SPOP (inverse), TP53, cell-cycle, WNT (inverse), andMYC pathways. Overall survival (OS) rates varied from 2- to 4-fold according toalterations in the AR, SPOP (inverse), WNT (inverse), and cell-cycle pathways.PI3K pathway alterations were not associated with prognosis.

Docetaxeland next-generation AR axis-directed therapies have been shown to prolong OS, butit remains uncertain which patients benefit the most from intensifiedtherapies. We did not find any obvious genomic reason to explain thedifferences in docetaxel sensitivity between high- and low-volume disease, DrKantoff said.

Theauthors pointed out that genomic landscape studies of tumor DNA profiling inprostate cancer in general have excluded metastatic castration-sensitive tumors.Instead, most studies have focus on localized disease or metastaticcastration-resistant disease.

DrAbida and his colleagues acknowledged that their study has inherent biases becauseit was hospital based and enrolled patients at an academic referral center.

Moleculardeterminants of castration resistance or survival in patients with mHSPC have beenunclear, but the new study sheds new light on molecular alterations associatedwith poor outcomes in men with mHSPC, particularly alterations in the AR, cellcycle genes, MYC, and TP53 genes, said Joshi Alumkal, MD, the Leader of theProstate/Genitourinary Medical Oncology Section and Associate Division Chieffor Basic Research in the Hematology-Oncology Division at the University ofMichigan School of Medicine.

Severalrandomized phase 3 clinical trials now show a benefit of escalating treatmentin men with mHSPC by adding novel AR-targeting agents or chemotherapy plusmedical castration versus medical castration alone, Dr Alumkal said. Whetherthe addition of any of these specific agents to medical castration isassociated with improved outcomes in patients with poor-risk molecularalterations identified by the new study is a critical next question, he said.

Urologiconcologist James Mohler, MD, Senior Vice President for Translational Researchat Roswell Park Comprehensive Cancer Center in Buffalo, New York, said the new study found relativelysmall differences among the clinical phenotypes, but that is not surprisingbecause the temporal differences in the evolution of tumor biology occur overlong periods of time, much of which precedes clinical presentation. The hazardratios for association between mutational analysis and oncologic outcome insome cases were statistically significant, but are so small as to not beclinically significant. Part of the reason for this may be that prostatecancer, once metastatic, is so complex that no single mutation or single genepathway is driving growth and hence targetable at a high rate beyond the long provenbenefit from androgen deprivation therapy, Dr Mohler said.

Theresults reported by these authors may be disappointing to many clinicians, butare important because they represent a comprehensive analysis of mCSPC. Theauthors appropriately acknowledge that better tumor sampling and morecomprehensive genetic analysis and larger numbers of patients may be requiredto find any benefit to genomic or somatic sequencing, Dr Mohler said. I amafraid that these limitations are not just of their work but a biologicallimitation of aggressive prostate cancer, which makes improving treatment ofadvanced prostate cancer in an individual patient extremely challenging.

Reference

Stopsack KH, Nandakumar S, Wibmer AG, et al. Oncogenic genomic alterations, clinical phenotypes, and outcomes in metastatic castration-sensitive prostate cancer [published online March 27, 2020]. Clin Cancer Res. doi: 10.1158/1078-0432.CCR-20-0168

Originally posted here:
Genomic Alterations Linked to Outcomes in mCSPC - Renal and Urology News

Indians have some genetic advantage, but these are still early days to come to any conclusion

The fewer-than-expected cases positive to the novel coronavirus (SARS-CoV-2) in Indiahave spawned severaltheories, one of them being,Indians being immune to the virus.

It is theoretically possible as Indians are constantly exposed to microbes that keep the immune system primed, destroying pathogens attempting to attack. This is why children in very clean environments fall sick at the slightest exposure to a pathogen a concept known as the hygiene hypothesis.

Indians have some genetic advantage as well: Theyhave evolved to gain more genes that protect against viral infections, according to Rajalingam Raja, director of Immunogenetics and Transplantation Laboratory at the University of California in San Francisco, US. He said:

These genes enable natural killer (NK) cells, a type of white blood cells in our body that provide a first line of defense against viral infections

Two families of genes KIR genes and HLA genes playa part in this protective function. Indians have more KIR genes than the Chinese and caucasians. This could makeIndians more immune to the virus, according to Raja.

A similar mechanismprotectsbats from viruses like Ebola and SARS. Bats are immune since they have expanded gene families that enhance NK cell function, said Raja, who first wrote about NK cells in 2008 in journal Genes and Immunity.

This alone is, however, not enough to guide Indias strategy to fight the disease or even suggest that strict measures are not needed. A team of researchers from India and the US studied umbilical cord blood of children in the two countries and found differences. The findings were published in journal PLoS One in 2018.

We interpreted our study to suggest that Indian babies could be more susceptible to early-life infections if they had lower frequencies of certain immune cells, said Holden Maecker, director of the Human Immune Monitoring Center at Stanford University School of Medicine.

Persistent pathogen assault especially early in life is almost certainly detrimental. Thisisseen in the phenomenon of environmental enteropathy, where kids with poor sanitation and high enteric pathogen loadsdevelop malnutrition and stunting, Maecker said. But he agreed exposure to pathogens could equip the immune system better to fight new assaults like Zika or coronavirus, to an extent.

This was similar to the protective effect provided by latent tuberculosis. It was certainly possible that there was increasing resistance if not specific immunity to COVID-19 in certain genetic groups. It is difficult, however, to extrapolate this to all Indians who are a diverse collection of ethnic groups.

It is a balance and my guess is that its too soon to say where Indians as a whole will fall on this balance in terms of their sensitivity to COVID-19, hesaid.

Arguments about the Indian immune systemsare mostly speculative, according to Satyajit Rath of the National Institute of Immunology. He co-authored the 2018 study with Maecker.

I am yet to see any indication that COVID-19 will, in fact, turn out to be less prevalent and/or milder in India, since the epidemic is still in its early stages in the subcontinent, he said.

There are no publications, as of now, on the differential prevalence or outcome of COVID-19 among Indians and those of other ancestries worldwide.

Good nutrition, exercise and sleep can improve the immune system.

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COVID-19: Do Indians have higher immunity to novel coronavirus - Down To Earth Magazine

Families across the U.S. will get a portion of money from the federal government's sweeping $2 trillion stimulus package. But how much? USA TODAY

On the day some Americans could begin receiving stimulus checks from the federal government amid the coronavirus pandemic that has eroded the country's financial footing, economists surveyed by Bloomberg predict the Labor Department will report another 5.5 million initial claims for unemployment insurance.

A record 6.6 million people sought benefits for the report issued a week ago after 3.3 million claims, then a record, were reportedthe previous week.

Also Thursday, astronauts launched for the International Space Station after a "strict quarantine." And the Trump administration loosened restrictions on essential workers.

The U.S. death toll was nearing 15,000 early Thursday, with more than430,000 confirmed cases, according tothe Johns Hopkins University data dashboard. Worldwide, there are close to 1.5million confirmed cases and more than 88,500 deaths.

Our live blog is being updated throughout the day. Refresh for the latest news, and get updates in your inboxwithThe Daily Briefing.More headlines:

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A side of toilet paper to go?Some restaurants are serving up more than meals during coronavirus crisis.

Authorities say fake cops are taking advantage of coronavirus travel restrictions to illegally stop drivers.

Support these brands:Here are 20 retailers that are giving back during the pandemic

Much-awaited stimulus cash will beginflooding into millions of bank accounts next week in the first wave of payouts to shore up the nation's wallets.Millions of taxpayers will begin receiving the extra money to pay rent, groceries and other bills next week, or possibly as early as Thursday or Friday.The first group estimated to cover 50 million to 60million Americans would include people who have already given their bank account information to the Internal Revenue Service.

The first group also would includeSocial Security beneficiaries who filed federal tax returns that included direct deposit information, according to an alert put out today by U.S. Rep. Debbie Dingell, D-Mich. Dingell's announcementsaid the expectation is that the first direct deposits would hit inmid-April, likely the week beginning April 13.

Susan Tompor, Detroit Free Press

Congress has passed, President Trump has signed, a $2 trillion stimulus bill that includes checks to taxpayers. Here's how to see what you might get. USA TODAY

Attorney General William Barr called the restrictions in effect in many states to mitigate the spread of the coronavirus "draconian" and said Wednesday they should be revisited next month.Asked by Fox News host Laura Ingraham about the balance betweenreligious freedomsand the need to protect people, Barr said the federal government would be "keeping a careful eye" onstates' use of broad powers to regulate the lives of their citizens.

Officials, Barr said, should be "very careful to make sure...that the draconian measures that are being adopted are fully justified, and there are not alternative ways of protecting people."

Nicholas Wu

The new coronavirus began spreading in New York in February and came to the area via travelers from Europe, new research suggests.Two separate teams of scientists studying the genetics of the virus came to similar conclusions: People were spreading the virus weeks before the first confirmed case in New York.

"So far, the majority seem to be coming from Europe, and this is in part I think because there was a focus on stopping travel from China," Adriana Heguy, a geneticist at NYU Grossman School of Medicine, told AFP.Harm van Bakel, a geneticist at Icahn School of Medicine at Mount Sinai who led the other research team, told the New York Times: "The majority is clearly European."

The first case of the new coronavirus confirmed in New York came on March 1. On Jan. 31, President Donald Trump said he would restrictentry to the United States from those traveling from China. On March 11, Trump said he was restricting travel from Europe.

Ryan W. Miller

There probably wont be much let-up in the nations grim tally of job losses, at least in the short term, as the coronavirus pandemics toll on the economy mounts.

Economists surveyed by Bloomberg estimate the Labor Department will report Thursday that 5.5 million Americans filed initial applications for unemployment insurance last week, below the record 6.6 million who sought benefits the previous week. Jobless claims provide the best measure of layoffs across the country.

The figures are so outsizedthat forecasting them has become something of a crapshoot. Michelle Meyer, chief U.S. economist of Bank of America Merrill Lynch, predicts the latest initial claims total Thursday will be 6.5 million, and JPMorgan Chaseestimates anall-time-high of 7 million.

Paul Davidson

Another trial is underway to test the safety of a possible vaccine for the new coronavirus, and those who fear needles may be in luck: It uses a skin-deep shot that would feel like a small pinchinstead of a deep jab.The trial aims to give 40 healthy volunteers in Philadelphia and Kansas City, Missouri, two doses of the potential vaccine, INO-4800, four weeks apart.

Similar to another clinical trial that began testing for safety in Seattle last month, the potential vaccine does not rely on using the virus itself. Inovio Pharmaceuticals' trial, instead, injects a piece of synthetic DNA with a section of the virus' genetic code. The Seattle trial relies on messenger RNA. After the shot,volunteers are given a brief electrical pulse that allows the synthetic DNA to more easily enter the body.

Dozens of other potential vaccines are being developed around the world, but it could be more than a year to 18 months before a vaccine is widely available, public health officials have said.

- Ryan W. Miller

The European Union could collapse if it fails to come together over financial challenges presented by the coronavirus, Italy's prime minister said. Giuseppe Conteand some other EU leaders are pressingmore frugal members of the bloc to issue so-called "corona bonds" - sharing debt that all EU nations would help to pay off. The Netherlands is among nations that haveopposed the plan.

"If we do not seize the opportunity to put new life into the European project, the risk of failure is real," Conte told the BBC.

Conte also saidItaly may start to gradually ease the world's most restrictive national lockdown. The number of new COVID-19cases, hospitalizations and deaths have started to decline across the country in recent days. Italy has reported more than 17,000 deaths, the most of any nation, and almost 140,000 confirmed cases.

The coronavirus pandemic is forcing people to stay home, but three astronauts are set toexperience a different type of isolation and quarantine in space. NASA astronaut Chris Cassidy and his fellow crewmates, Russia's Anatoly Ivanishin and Ivan Vagner,blasted offaboard the Soyuz MS-16 spacecraftat 4:05 a.m. ET from Kazakhstan for a six-hour journey to the International Space Station.

Russian space officials have taken extra precautions to protect the crew during training and pre-flight preparations as the coronavirus pandemic has swept the world. Speaking to journalists via video link Wednesday, Cassidy said the crew has been in a very strict quarantine for the past month and so in good health.We all feel fantastic, he said.

Associated Press

U.S. stocks were poised to give up modest ground when markets open Thursday, one dayafter the Dow Jones industrial Average raced 779.71 points higher to close at23,433.57. The Standard & Poors 500 rose 3.4% Wednesday to end at 2,749.98, driven by gains in beaten down energy, real estate and utility shares.The broad index has jumped nearly 23% since it hit a low two and a half weeks ago.

Shares were mixed in Asia on Thursday after a 3.4% gain on Wall Street as investors chose a positive focus for data about the coronavirus outbreaks trajectory.

The prospect for progress in talks among oil producers was a big driver of Wednesday's rally, along with the signs of virus infections leveling off in several global hotspots and increased clarity in the U.S. presidential race, said Adam Taback, chief investment officer for Wells Fargo Private Bank.

Prime Minister Boris Johnson spent a third night in intensive care beingtreated for coronavirusand is instable condition and "improving," his office said.Johnson had a "good night" in the hospital, a Downing Street statement said.However, Britain's leader, 55, is still on oxygen and has handed over day-to-day operations of his government Foreign Secretary Dominic Raab.

Johnson's wife, Carrie Symonds, is pregnant and also suffered symptoms consistent with the coronavirus. Earlier this week, Symonds tweeted that she was feeling stronger and "on the mend."

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In a first, small step toward reopening the country, the Trump administration issued new guidelines to make it easier for essential workers who have been exposed to COVID-19 to get back to work if they do not have symptoms of the coronavirus.

Dr. Robert Redfield, director of the the Centers for Disease Control and Prevention, announced Wednesday at the White House that essential employees, such as health care and food supply workers, who have been within 6 feet of a confirmed or suspected case of the virus can return to work under certain circumstances if they are not experiencing symptoms.

Associated Press

The Centers for Disease Control and Prevention has new guidance for essential workers as it takes a small step toward reopening the country. (April 8) AP Domestic

According to new documents released Wednesday by the House Oversight Committee, 90% of the federal personal protective equipment stockpile had been depleted as the Health and Human Services Department made its "final shipments" of N95 respirators, surgical and face masks, face shields, gowns, and gloves.

The remaining 10%, HHS said, would be reserved for federal workers and would not be sent to the states.

The documents, which report the distribution of personal protective equipment to state and local governments, show that only11.7 million N95 respirator masks have been distributed across the nation, and only 7,920 ventilators have been distributed both small fractions of the estimated amount of protective equipment needed by frontline medical workers.

Nicholas Wu

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While governors, mayors and hospital officials conduct much-publicized life-and-death struggles to acquire ventilators, for most COVID-19 patients the oxygen-providing apparatuswill merely serve as a bridge from life to death.

Dennis Carroll, who led the U.S. Agency for International Development's infectious disease unit for more than a decade, told USA TODAY perhaps one-third of COVID-19 patients on ventilators survive.

But for many, ventilators represent their last chance."If you were one of the one-third, I suspect youd be very appreciative that that capability was available," Carroll said.

Some patients may be on a ventilator for only a few hours or days, but experts say COVID-19 patients often remain on the ventilators for 10 days or more.

John Bacon

Mapping coronavirus:Tracking the U.S.outbreak, state by state.

When will life return to normal? U.S.testing is too far behind to know, says one expert.

How the 50 states are responding to coronavirus:And why eight states haven't issued stay-at-home orders.

'Scotch tape and baling wire':How some hospitals and companies are responding to meet America's ventilator shortage.

You're not 'too busy' to stay active: Health experts worry about inactivity during coronavirus quarantine.

Contributing: Paul Davidson, USA TODAY; The Associated Press

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Coronavirus live updates: Stimulus checks on the way; New York's outbreak may have come from Europe; US death toll nears 15,000 - USA TODAY

Why the two-metre rule may not be enough

SOCIAL distancing guidance is to keep two metres away from people we dont live with. This rule is thought to be based on experiments from the 1930s that suggested droplets released from coughs and sneezes can travel between one and two metres.

But this understanding may be outdated. In an experiment led by the Health and Safety Executive, a cough from a medical manikin called Violet provides a graphic illustration of just how easily and how far coronavirus particles can spread.

In the demonstration, Violet coughs up a liquid laced with a dye that shows up under ultraviolet light. The dye is meant to reveal how droplets containing coronavirus particles are propelled through the air when we cough.

"You see thousands of droplets coming out of Violets mouth, with some reaching the ceiling and the far wall, which is at least two metres away," says paediatrician Dr Guddi Singh.

"Some of these droplets land on my hand, even though I am not in the direct line of the cough. If these droplets contained the virus, I would be infected. It is incredibly contagious.

"The experiment shows me why we need social distancing of at least two metres," she says. "But even at that, you are just on the fringe of where the spread could be happening."

Indeed, new research published in the Journal of the American Medical Association suggests that two metres may not be nearly far enough; that coronavirus particles can be propelled up to eight metres by sneezes and six metres by coughs.

Some experts suggest that the larger droplets in saliva and mucus the ones believed to carry Covid-19 will fall safely to the ground within two metres. However, the US researchers said their experiment calls into question our understanding of what a safe distance might be.

Another report even suggests we may have more than coughs and sneezes to worry about. The prestigious National Academy of Sciences in the US recently warned that the virus may also be spread by the fine mist we produce when we talk and breathe.

One study suggests this can spread genetic material from the coronavirus more than two metres away from patients. This raises the possibility that the virus can linger in the air and potentially infect someone who walks by later.

All this research has prompted the World Health Organisation to start a review of its advice on the use of face masks.

Dilemma of the silent spreaders

THE spread of Covid-19 by people who arent showing symptoms is one of the reasons the virus is so dangerous. A study published in the journal Science concluded that 86 per cent of cases have either no symptoms or only very mild ones.

Countries such as Iceland and South Korea have reported a huge number of silent spreaders. In South Korea, 40.2 per cent of those aged 20 to 29 fell into this bracket.

It is not known why some people dont show symptoms, but it may be due to differences in their genetics.

How long does the virus survive?

WHETHER you have symptoms or not, the virus will be released from your respiratory system into the air and the droplets can "last for many hours on different surfaces which we may then touch", says Dr Singh.

"A recent study in the New England Journal of Medicine revealed the virus can survive suspended in the air for up to three hours. It can stay on cardboard for 24 hours and plastic for 72 hours."

This, says Dr Singh, could have implications for online shopping.

"In countries that seem to have managed the outbreak pretty well, such as Singapore and Taiwan, all deliveries are treated very seriously because it is clear that this could be another mode of transmission.

"With deliveries, there is advice that plastic items should be wiped down with soap and water."

Other experts say you are unlikely to reach every nook and cranny, so would be better off keeping your hands clean.

Its not just a cough and fever

THE official advice is that the two main symptoms of Covid-19 are a high temperature and a "new and continuous cough". Indeed, data gathered by the WHO in February on more than 55,000 confirmed cases in China showed a fever to be the most common symptom, occurring in 87.9 per cent of cases, followed by a dry cough (in 67.7 per cent).

Other symptoms listed included fatigue, coughing up phlegm, sore throats, headaches and diarrhoea and vomiting.

In the last ten days of the pandemic, a new symptom has emerged: loss of sense of smell. Data collated by ENT UK, which represents ear, nose and throat specialists, suggests this inability to smell and, often, to taste may be the very first sign.

Indeed, a new report from Kings College London points to it being one of the most common symptoms.

Younger people are at risk too

It is known that older people and those with underlying conditions such as type 2 diabetes and heart and lung diseases, such as chronic obstructive pulmonary disease (COPD), are more likely to become severely ill with coronavirus. A report in The Lancet last week where researchers from Imperial College London analysed data from China showed how the risks of serious illness and death rise sharply as we get older.

While a 20-year-old has about a 1 per cent chance of their illness being so severe that they are hospitalised, the risk rises to around 4 per cent for someone in their 40s; 8 per cent for someone in their 50s; and 19 per cent for the over-80s.

Yet, younger people are not invincible. Data from NHS England shows that while the vast majority of the almost 5,000 deaths in England have been in the over-60s, 396 younger people under 60 have lost their lives to Covid-19.

It is possible some peoples genetics makes them more vulnerable. Another theory revolves around the viral load the amount of virus someone is initially exposed to.

With some viruses, the more you breathe in, the sicker you get, which could explain why young nurses who are in close contact with lots of sick patients are dying from coronavirus.

The power of handwashing

In 2018, mathematician Dr Hannah Fry, who presents the BBC2 show with Dr van Tulleken, simulated a pandemic of a deadly flu virus. Her experiment revealed how quickly the contagion could be slowed simply by handwashing.

Washing hands an extra five-to-10 times a day would halve the number of people who caught the virus in the next 100 days, she says.

"The way that pandemics spread is all exponential, which means tiny things can have a massive impact. Things like handwashing, done properly, can genuinely make a difference," says Dr Fry.

:: Coronavirus, Horizon Special, BBC2, Thursday April 9, 9pm.

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Two metres may not be nearly enough: What scientists now know about the virus - The Irish News

Imagine generating a vaccine for the novel coronavirus from your immune system.

The virus that causes COVID-19 has swept the globe with about 1.3 million infections and 70,000 deaths through Sunday evening.Development of a widely available vaccine can take a year or more while a virus continues its rampage.

Key to the race to develop a vaccine for the new coronavirus is a technology that uses the virus' genetic code to essentially persuade your body to make its own vaccine.

This techniqueis faster than egg-based manufacturing, which produces the majority of annual flu vaccines and led to delays in distributing a vaccine forH1N1 during the 2009 pandemic.

And it's enablingapossible vaccine for the new coronavirus to be developed in record time.

Coronavirus updates: Get the latest in USA TODAY's live blog

Its quicker to get started, said Clem Lewin, who is working onvaccine candidates for the manufacturer Sanofi Pasteur. All you need is the blueprint for the protein."

Testing still will take time. Scientists must determine whether any of several vaccine candidates fight the virus effectively. If so, they need to determine the proper dose. This tinkering is what could take a year or more.

When the first potential vaccine from the manufacturer Moderna was injected into people on March 16, Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, said he believed the coronavirus vaccine was being developed at a record pace. It took 63 days to go from identifying a viruss genetic sequence to testing a vaccine in people.

Scrambling egg-based production

Several manufacturers pursuing a vaccine for the latest coronavirus have been aided by a technological innovation.

The method that Moderna, Sanofi and others are pursuing is different from traditional vaccinations, in which a weakened or dead version of the virus is introduced into the body, triggering itto createantibodies that would attack the live virus should the person be exposed to it.

In the new approach, pieces of messenger RNA that hold the chemical template of a spike protein from the SARS-CoV-2 virus are injected into a human, said Mark Slifka, a professor of viral immunology at Oregon Health and Science University in Portland, Oregon.

The spikes are what the virus uses to attach to a human cell the first step in sickening someone.

In response to the injection of those molecules, the cells in the body produce the spike protein encoded by that mRNA. That triggers the body tomountan immune response to that viral protein, just as in traditional vaccines.

Essentially, the patient makes their own vaccine, says the narrator of a Moderna video about the vaccine.This cuts out the middleman.

Fauci said volunteers would be given two injections of the potential coronavirus vaccine, the second after 28 days. The doses are 25 milligrams, 100 milligrams and 250 milligrams, he said.

The individuals will be followed for one year both for safety and whether it induces the kind of response that we predict would be protective, Fauci said.

Moderna, the manufacturer conducting the initial tests, projected the first commercially available vaccine in 12 to 18 months. A corporate filing March 23 said CEO Stephane Banceltold Goldman Sachs it is possible that under emergency use, a vaccine could be available to some people, possibly including healthcare professionals, in the fall of 2020.

Why change the menu from reliable eggs?

Most flu vaccines are produced from fertilized chicken eggs, a decades-old process that takes four to five months.The mRNA process ismuch faster.

Delays in producing an H1N1 vaccine spurred health officials to urge development of other technologies, according to a Government Accountability Office report.

Its a state-of-the-art technology for the 1950s, Luciana Borio, then director for medical and biodefense preparedness at the National Security Council, said at a 2018 conference on the 100th anniversary of the Spanish flu pandemic.

A New England Journal of Medicine review of the response to H1N1 found that 78 million doses of the vaccine were eventually produced for 70 countries worldwide, but only after two waves of the illness worldwide.

The most serious operational shortcoming ...was the failure to distribute enough influenza vaccine in a timely way, the report said. The cause: distribution problems, "a shortfall in global vaccine-production capacity and technical delays due to reliance on viral egg cultures for production.

Developing a vaccine is laborious, said Harvey Fineberg, a former president of the U.S. Institute of Medicine and former dean of the public-health faculty at Harvard University.

One step is confirmingthat a possible vaccine doesn't causebad reactions in patients. Then scientists examine how much vaccine is required for an antibody response. And they must verify the vaccine actually protects against infection, which is why it's ideal to test during an outbreak.

All those steps come after scientists identifythe genetic sequence to target for a vaccine.

Its like saying,'Ive got my architectural plans my house must be ready to move into,' Fineberg said. There are a lot of things you need to do between now and being ready to open the door.

Manufacturers work with government

The manufacturers pursuing coronavirus vaccines are working closely withthe Centers for Disease Control and Prevention, the Food and Drug Administration, the National Institute of Allergy and Infectious Diseases and the Biomedical Advanced Research and Development Agency.

Moderna is working on 13 potential vaccines. Sanofi is working on two candidates:an mRNA candidate with the company Translate Bio and another option in collaboration with the Biomedical Advanced Research and Development Agency.

Other companies are pursuing other technologies. GlaxoSmithKline is working with China-based Clover Biopharmaceuticals through a different process to produce a cell-based vaccine.

Johnson & Johnson, which is working on several possible vaccines,announced last week it wouldinvest$1 billion for vaccine research, development and testing. The company said it could produce 1 billion doses of a vaccine when the time comes.

Sen. Chris Coons, D-Del., said $3.5 billion in the coronavirus spending packagewill help develop manufacturing technologies to ensure a robust, agile, U.S.-based supply chain of vaccines, therapeutics, and active pharmaceutical ingredients.

The biggest challenge we face in the United States is not developing a vaccine, tricky as that step is, Coons said in a statement. Its that we lack the domestic manufacturing capacity to quickly produce a vaccine once its proven and deliver it to the American people.

Lewin of Sanofi said the global health emergency spurred manufacturers to try different technologies.

We and all the other manufacturers are working as quickly as possible to accelerate these programs while ensuring the vaccine is safe and effective, Lewin said. It isnt business as usual for anybody.

What about changes to flu vaccines?

The technology used todevelop a coronavirus vaccine wont affect the annual flu vaccine because they are different viruses requiring different approaches. But evenbefore the pandemic,steps were underwayto hasten changes to the flu vaccine.

President Donald Trump signed an executive orderin September calling onmanufacturers to move away from egg-based vaccines because of critical shortcomings, including the months they take to produce. The order anticipated a pandemic more lethalthanthe 1918 Spanish flu, which killed 675,000 Americans.

William Schaffner, professor of infectious diseases at Vanderbilt University, said one reason tochange vaccine productionis that growing the vaccine in eggs allows mutationsthat make it less effective.

People were working on this already, Schaffner said. That sort of commitment, a presidential commitment, plus the moneys that go with it, really put the pedal to the metal for future research.

Egg-based vaccine manufacturing has been reliable. Developing another process would require a multimillion-dollar investment in an industry with small profit margins, Schaffner said.

Moving away from egg-based production is not like flipping a switch, he said. Im sure all the manufacturers are all thinking about this, but how and how quickly they do it is another matter.

Other options include cell-based and recombinant processes. A cell-based vaccine is grown in a mammal's cells, such as kidney cells from monkeys or dogs, rather than in a hen's eggs. A recombinant vaccine is created synthetically from the DNA, or genetic instructions, of a protein from the flu virus. The DNA is then combined with a baculovirus, which infects invertebrates.

Other changes could address vaccine delivery, perhaps moving from injections to pills or skin patches, Schaffner said.

A loftier goal is to develop what is called a universal vaccine, which could last five years at a time. Such a vaccine could be administered any time of year during a doctor's visit, rather than just in the fall.

Doing that would require changing how the vaccine attacks the flu virus, whichis shaped like a sphere with lollipops protruding from it. Vaccines so far have targeted the candy at the end ofthe lollipop, which changes every year.

A vaccine that targetsthe stem of the lollipop could offer protection for years, Shaffner said. If you get vaccinated, youre vaccinated against a whole series of different influenza viruses,Schaffner said.

The coronavirus pandemic has come during a severe flu season. This years vaccine is about as effective as usual, according to a Centers for Disease Control and Prevention study of cases through Feb. 8. The study found the severity for people up to 49 years old including hospitalizations was worse than other recent seasons, including the severe year of 2017-2018.

Current influenza vaccines are providing substantial public health benefits,"said the study in CDCs Morbidity and Mortality Weekly Report."However more effective vaccines are needed."

Contributing:Elizabeth Weise

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A coronavirus vaccine is being developed in record time. But dont expect that technology to speed up flu vaccines yet. - Columbia Daily Herald

This research was partly funded by the Federal Canadian government, to support the development, testing and implementation of ways to manage the pandemic. Rumours have been circulating social media platforms at the speed of light, discussing the imminence or the impossibility of a real cure. Here, we discuss the ongoing research of a trial drug that is biologically capable of preventing fatalities from Coronavirus.

The answer is by closing the door that COVID-19 uses to enter the cells of your body.The door is the ACE2 protein on the surface of the cell membrane.

SARS-CoV-2 is the virus that causes COVID-19, which is commonly known as Coronavirus. During the last major outbreak of SARS, a similar viral respiratory illness that caused global devastation in 2003, it was Dr. Penninger and his colleagues who discovered that the ACE2 protein was the key receptor for SARS. In further research, he discovered that this protein was linked to a resultant cardiovascular disease and lung failure.

The ACE2 protein is where the spike glycoprotein of SARS-CoV-2 enters the human cell, like a door being broken down. The world is looking for a cure but there is no clinically proven antiviral treatment right now, or any treatment focusing on protecting the ACE2 receptor. This means that late-stage COVID-19 can be a fatal situation for those who are already experiencing other immune or lung issues.

The NHS defines antiviral treatment as: a type of medication used specifically for treating viral infections. They act by killing or preventing the growth of viruses.

The researchers here are not proposing a treatment that could kill the virus they are exploring the potential of highly calculated self-defence, on a microscopic level. What if those cellular doors were never broken down by the invading COVID-19 forces, because they were hidden or protected?

Dr. Josef Penninger, the UBC scientist leading this study, said:

There is hope for this horrible pandemic.

The study found that in cell cultures, hrsACE2 inhibited the early stages of COVID-19 load by a factor of 1000-5000. The researchers grew organs of blood vessels and kidneys from stem cells, to quickly test their ideas on a functioning human being.

Nria Montserrat, ICREA professor at the Institute for Bioengineering of Catalonia in Spain, said:

In these moments in which time is short, human organoids save the time that we would spend to test a new drug in the human setting.

The researchers showed that in these organs, the virus can directly infect and duplicate itself in the tissues of the blood vessel and kidney. This gave them valuable insight into how COVID-19 cases that are severe present with multi-organ failure, with evidence of cardiovascular damage.

It was found that clinical grade hrsACE2 reduced the infection in these engineered organs.

Dr. Art Slutsky, a scientist at the Keenan Research Centre for Biomedical Science of St. Michaels Hospital and professor at the University of Toronto, said:

Our new study provides very much needed direct evidence that a drug called APN01 (human recombinant soluble angiotensin-converting enzyme 2 hrsACE2) soon to be tested in clinical trials by the European biotech company Apeiron Biologics, is useful as an antiviral therapy for COVID-19.

Apeiron Biologics write that they are currently planning a clinical pilot study in China with COVID-19 infected patients, whilst evaluating options for further clinical development. APN01 was previously being used for Acute Lung Injury and Pulmonal Arterial Hypertension, for which the company currently have APN01 in Phase-2 clinical development. It is possible, given the existing Phase-2 level of development, that the next clinical trial for COVID-19 could automatically go to Phase-3. The length of Phase-3 clinical trials in Canada are usually one to three years, which involves around 1000-3000 patients. After that, the regulatory review can take anything between six months to two years.

However, given the global urgency, funding from Canadian government and clinical trials being held in China, it is highly likely that development of APN01 will be fast-tracked. We reached out for comment to the biotech company about possible timelines but have received no response at the time of publishing.

Penninger, professor in UBCs faculty of medicine, director of the Life Sciences Institute and the Canada 150 Research Chair in Functional Genetics at UBC said:

This work stems from an amazing collaboration among academic researchers and companies, including Dr. Ryan Conders gastrointestinal group at STEMCELL Technologies in Vancouver, Nuria Montserrat in Spain, Drs. Haibo Zhang and Art Slutsky from Toronto and especially Ali Mirazimis infectious biology team in Sweden, who have been working tirelessly day and night for weeks to better understand the pathology of this disease and to provide breakthrough therapeutic options.

The virus causing COVID-19 is a close sibling to the first SARS virus.

Our previous work has helped to rapidly identify ACE2 as the entry gate for SARS-CoV-2, which explains a lot about the disease. Now we know that a soluble form of ACE2 that catches the virus away, could be indeed a very rational therapy that specifically targets the gate the virus must take to infect us. There is hope for this horrible pandemic.

The findings of the study have been published in Cell.

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Researchers test drug that stops early stages of COVID-19 - Open Access Government

THERES a 70 per cent chance youre going to get a mum without MS for the first time.

Those were the words Amanda Weyman-Jones told her daughter before they hopped on a plane, in a last ditch-attempt for Amanda to take her future back.

In January, Amanda and daughter Chloe travelled halfway across the globe to Moscow, Russia for a life changing and experimental treatment in hopes it would effectively stop her three decade battle with multiple sclerosis in its tracks.

The trip was made possible with the support from the Roma community who banded together to help Amanda raise $80,000 to pay for the treatment only available in the Russian capital.

And according to Amanda, she has already seen a massive improvement with her condition.

Im walking and I would say I have improved 70 per cent already, and its only expected to get better as time goes on, the 58-year-old mother of six said.

They say that the treatment gives you an 80 per cent (chance) of curing your MS and at the moment, I feel like Im in that 80 per cent Im feeling really good about my chances.

Amanda underwent an experimental procedure called Autologous haematopoietic stem cell transplant (AHSCT) treatment, which rebuilds the patients immune system.

Seven weeks on and Amanda says she feels like a new person, and has been walking around the football field everyday, which she states is a miracle as she couldnt even walk to the field before the treatment.

Ever since returning to Roma from Russia in February, all she has wanted to do is shout from the rooftops that others living with MS can also have their lives changed.

I heard about a man on a property in Blackall with MS and hes young so I want him to know he doesnt have to have this disease, you can get better, Mrs Weyman-Jones said.

This treatment gives you that infinity with people. Its life saving stuff.

Amandas brother Hayward and sister Diana were both diagnosed with MS too; Hayward died last year, and Diana is now in a wheelchair.

All too familiar with the devastating effects of MS, Amanda is determined to not become a burden on her loved ones.

Amanda who has Primary Progressive MS was given an Expanded Disability Status Scale (EDSS) score of 4.5 which notes a limited walking mobility to approximately 300m without aide prior to treatment. With no action taken, she would probably have continued to progress until she was wheelchair bound. The EDSS is scored zero to 10, with 10 marking a person has died from MS.

Now, with more improvements expected to continue in the next six to 12 months, Amanda is hopeful her quality of life will improve and once her immunity has built up, to continue working at the family-owned-and-run Overlander Motel.

I will be forever grateful to Dr Frederinco, the brilliant medical team in Russia, Roma, its local businesses and the wider community for blessing me with a new life, Amanda said.

Through the generosity and support by all, I have realised how lucky I am to be surrounded by such a caring community.

Amanda said she knew that while there is a long road ahead of her, every passing day she is more feeling more hopeful.

I was told that recovery can be like a rollercoaster, so I will accept the bad days and make sure I remember the good, she said.

My walking is slowly getting safer and less hazardous to myself . and to all other pedestrians. Every morning I wake up, knowing that every days a better day.

I am a new person, it is just a miracle.

Stats about MS

With MS Queensland aware of nearly 4000 people living with Multiple Sclerosis in Queensland and over 25,600 people in Australia living with the neurological condition.

Most people with MS in Australia experience their first symptoms between 20 and 40 years of age, with about three quarters of people living with MS, female.

MS is not considered a classic genetic disease in that there is not one single gene that causes the condition. Rather, there are more than 200 different known genetic factors which contribute to the risk of developing MS. It has been estimated that genes may account for around half of the risk for MS, and those with a family history of MS are at greater risk than the general population. Even so, the majority of people with a family member with MS will not develop the disease so genes on their own are not enough.

MS is caused by a complex interaction between a persons genetics and environment factors.

Autologous haematopoietic stem cell transplant (AHSCT) is an immunosuppressive chemotherapy treatment combined with reinfusion of blood stem cells to help rebuild the immune system.

AHSCT has been used for decades for the treatment of blood cancers. However in the past ten or so years a number of international observational studies of several hundred patients have been published with some patients being followed for five to eight years.

The treatment consisted of four days of stimulation before the stem cells were collected and then Amanda was pumped full of high dose chemotherapy.

Amanda then had a rest day, and on January 29, her harvested stem cells were returned to her MS ravaged body, signalling the rebirth of her immune system with no memory of MS.

After that she was given daily steroid infusions and was put into isolation for six nights before one final dose of chemotherapy.

Response from MS Queensland about the treatment

CEO of MS Queensland Zane Ali said MS Queensland and MS Research Australia are continuing to support Australian research in the use of AHSCT to treat multiple sclerosis.

Rigorous evidence for the efficacy and safety of AHSCT in relation to other MS therapies, and the most appropriate circumstances for its use, is required for Australian hospitals and clinicians to provide this intervention with equity and with greater confidence in the potential outcomes, he said.

Australian hospitals and doctors are likely to recommend AHSCT as a possible treatment only if the other approved MS therapies are not working for an individual with MS or cannot be used in an individual for other reasons.

Despite Amandas MRI revealing her Central Nervous System was so progressed (with 35 lesions or more on the spine), she met the criteria for the treatment because of her mobility.

You have to be at a very healthy besides having MS, patients are tested from head to toe when they first arrive in hospital to ensure that they dont have any cancers or illnesses that could effect the viability of the treatment, said daughter Chloe.

The doctor was surprised after he saw how mobile mum still was considering the damage that he saw in her brain.

People arent accepted all of the time, some are told before they go and some are only told after all of the testing is completed in Moscow, then they are then sent home. International studies also suggest AHSCT does not halt or reverse progressive forms of the disease, and is therefore unlikely that

AHSCT would be recommended as a treatment for patients with secondary progressive or primary progressive MS.

Currently the treatment is provided in Australia through two observational clinical trials, at St Vincents, Sydney and Austin Health, Melbourne and by a small number of other centres on a case-by-case basis.

These centres have strict eligibility requirements that have been set by the hospital ethics committees and may only apply to limited numbers of patients with MS, Mr Ali said.

It is for this reason patients need to be referred to these centres by a neurologist, who can provide a detailed clinical history and MRI findings, Mr Ali said.

Mr Ali said that data from the large European Bone Marrow Transplant Registry suggests that in approximately 55 per cent of people with MS, treated with a range of different chemotherapy regimens, at three years of follow-up, inflammatory disease is halted with no evidence during the follow-up period of relapses, active brain lesions or disability progression.

After five years approximately 45 per cent of people remain progression free.

This case series included patients with both relapsing remitting and progressive disease, he said.

Other smaller studies have shown similar results, with remission of disease seen in these studies in at least 63 per cent of patients followed for a minimum of three years.

Most studies also show that the risk of disease activity returning gradually increases over longer periods of follow-up.

Mr Ali said in some but not all, of the people with MS who respond to AHSCT, some reversal of disability has been noted in some studies.

Other patients may continue to experience disease activity and disability progression (worsening) despite treatment with AHSCT, he said.

In people with progressive forms of MS or relapsing remitting MS of longer duration, the benefits of the procedure have been much less clear and accumulation of disability usually continues.

Amanda said they chose Moscow for the treatment because despite other countries offering the experimental procedure, after thorough research they found Russia had the highest rate of treatment success.

They accept advanced progressive MS where most of the other clinics offering it only treat relapsing remitting MS, she said.

I was still on my feet (only just) but people went over in wheelchairs, walkers, walking sticks and many were older than me.

For Chloe, who is training to become a nurse and who spent every spare moment researching AHSCT treatment said while they mostly compared the options available in Mexico and Russia, Russia stood out to them because it was cheaper and they had more experience.

One of the major influencing factors was that in Mexico patients stayed in a complex with they carer and in Russia patients stayed in a hospital, so we felt more reassured knowing that mum would have 24 hour care provided to her at the touch of a buzzer, she said.

Great lengths of a loving daughter

Although Amanda has lived with MS for 34 years, she feels like she is one of the lucky ones.

None of this would have been possible without Chloe. Her drive and determination surprises me every day, she said.

Researching, booking, fundraising and organising the whole trip, proves to me that I am the luckiest mum on earth.

Chloe was the driving force behind the push for treatment and the GoFundMe campaign which raised over half the $80,000 goal was with her mum every step of the journey.

I have found spending a month in Russia very interesting, the first couple of weeks for easy, but after that I just wanted to come home to Australia, the 19-year-old said.

Every day I would go and visit Mum in the morning and stay there with her until dark and then head on back to the hotel, I basically just did that every day.

I made some great friends with some other patients carers and so often we would catch up at the end of the day to recuperate and support each other.

Although the month spent away from her loved ones began to take its toll, Chloe has high hopes for the future.

It was very draining being over there, I felt like I wasnt doing much but I was just always so tired, she said.

Its amazing to see how quickly mum is healing after the treatment, but it will take some time to see what the true outcome for her is going to be.

In the end, we dont know what the future holds for mum and her MS, we are just thinking positively and hope that we see improvements over the next 12 months.

We feel very lucky that we had the opportunity to go over and are now advocating for other people to have the treatment as well.

Chloe and Amanda Weyman-Jones sightseeing in Moscow before the treatment began.

During the treatment.

Amanda Weyman-Jones with Greta and Theresa who were also going through the treatment.

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Roma woman tells of her 'life-changing' MS treatment - Chronicle

The Leukapheresis market research report is required to show a gigantic development inside the upcoming years. The investigators likewise have dissected downsides with on-going Organic Semiconductor patterns and in this manner the open doors that are giving to the expanded development of the business. The report gives the viewpoint of this aggressive scene of worldwide markets. The report passes points of interest that started from the examination of the focused on market

leukapheresis market is expected to rise from its initial estimated value of USD 19.9 million in 2018 to an estimated value of USD 36.1 million by 2026 registering a CAGR of 7.7% in the forecast period of 2019-2026. Leukapheresis is a procedure used for separating white blood cells from a sample of blood. It can be performed to reduce the count of very high white blood cell, to attain cells for various research purposes and to obtain autologous blood cells for further transplant back into patient. It is a type of apheresis, used for separating out a particular constituent of blood and to return the remaining part back to the circulation.

Leukapheresis Market 2027 Top Players (Market Analysis, Opportunities, Demand, Forecasting)

Click HERE To get SAMPLE COPY OF THIS REPORT (Including Full TOC, Table & Figures) [emailprotected]https://www.databridgemarketresearch.com/request-a-sample/?dbmr=global-leukapheresis-market

The titled segments and sub-section of the market are illuminated below:

By Type (Leukapheresis Devices, Leukapheresis Disposables),

Application (Research Applications, Therapeutic Applications),

End User (Blood Component Providers and Blood Centers, Academic and Research Institutes, Pharmaceutical and Biotechnology Companies, Hospitals and Transfusion Centers),

Geographical Insights:

In-depth qualitative analyses include identification and investigation of the following aspects:

The trend and outlook of global market is forecast in optimistic, balanced, and conservative view. The balanced (most likely) projection is used to quantify global extended reality market in every aspect of the classification from perspectives of Technology, Component, Device Type, Industry Vertical, End-user, and Region.

Competitive Analysis: Leukapheresis Market

The global leukapheresis market is highly fragmented and the major players have used different strategies such as mergers, partnerships, expansions, innovative product launches, agreements, joint ventures, acquisitions and others to increase their footprints in this market. The report includes market shares of leukapheresis market for global, Europe, North America, Asia Pacific, South America and Middle East & Africa.

Leukapheresis Market competitive landscapes provides details by topmost Key Players like

Asahi Kasei Medical Co. Ltd, Haemonetics Corporation, Terumo BCT Inc., STEMCELL Technologies Inc., Macopharma, Fresenius SE & Co. KGaA, HemaCare, Caltag Medsystem Ltd, AllCells, StemExpress, PPA, Key Biologics LLC, ZenBio Inc., Precision for Medicine Inc., BioIVT, Digital Pharmacist Inc., Lmb Technologie GmbH, Grifols, S.A, Bioelettronica and Kaneka Pharma Europe NV.

Browse in-depth TOC on Global Leukapheresis Market60- Tables220- Figures350 Pages

The Study Objectives of the Global Leukapheresis Market Research Report are:

Table of Content:

Chapter One: Global Leukapheresis Industry Market Research Report

Chapter Two: Industry Chain Analysis

Chapter Three: Global Leukapheresis Market, by Type

Chapter Four: Leukapheresis Market, by Application

Chapter Five: Global Leukapheresis Production, Value ($) by Region (2015-2020)

Chapter Six: Global Leukapheresis Production, Consumption, Export, Import by Regions (2015-2020)

Chapter Seven: Global Leukapheresis Market Status and SWOT Analysis by Regions

Chapter Eight: Competitive Landscape

Chapter Nine: Global Leukapheresis Market Analysis and Forecast by Type and Application

Chapter Ten: Leukapheresis Market Analysis and Forecast by Region

Chapter Eleven: New Project Feasibility Analysis

Chapter Twelve: Research Finding and Conclusion

Chapter Thirteen: Appendix

Read More: https://www.databridgemarketresearch.com/toc/?dbmr=global-leukapheresis-market

For each of the aforementioned regions and countries, detailed analysis and data for annual revenue (demand and production) are available for 2020-2027. The breakdown of all regional markets by country and the key national markets by Technology, Component, and Industry Vertical over the forecast years are also included.

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Leukapheresis Market Is Booming Worldwide | Asahi Kasei Medical Co. Ltd, Haemonetics Corporation, Terumo BCT Inc., STEMCELL Technologies Inc. -...

How does our immune system react to the coronavirus?

The coronavirus is like any other virus not much more than a shell around genetic material and a few proteins. To replicate, it needs a host in the form of a living cell. Once infected, this cell does what the virus commands it to do: copy information, assemble it, release it.

But this does not go unnoticed. Within a few minutes, the body's immune defense system intervenes with its innate response: Granulocytes, scavenger cells and killer cells from the blood and lymphatic system stream in to fight the virus. They are supported by numerous plasma proteins that either act as messengers or help to destroy the virus.

For many viruses and bacteria, this initial activity of the immune system is already sufficient to fight an intruder. It often happens very quickly and efficiently. We often notice only small signs that the system is working: We have a cold, a fever.

Read more:Sepsis a common cause of death from coronavirus

Fever and feeling weak: This is how our immune system makes itself felt.

Interferons are a subgroup of signaling proteins that are normally secreted by infected cells. SARS-CoV-1, which was responsible for the SARS epidemic in 2003, appears to have suppressed the production of one of these interferons and thus at least delayed the attraction of immune cells. To what extent this is also the case with SARS-CoV-2, the name given to the coronavirus behind the current pandemic, is still unclear. However, interferons support the body's own virus defense and are now being tested as a therapy in clinical trials.

At a certain point, however, the host response is so strong that its effect can be counterproductive. For example, numerous immune cells can enter our lungs and cause the membrane through which oxygen normally passes from the air into the blood to thicken. The exchange of gases is restricted, and in the worst case, ventilation may be necessary.

Sometimes the reaction can overshoot and be directed against healthy cells as well. This could also be the case with the novel coronavirus. So drugs are also being tested that suppress an excessive immune reaction and that are already known from the treatment of autoimmune diseases. The balance between protective and overly aggressive immune processes in dealing with the coronavirus is currently a big mystery. This must now be investigated, says Achim Hrauf, Director of the Institute of Medical Microbiology, Immunology and Parasitology at the University of Bonn.

Read more:World Health Day: What does the WHO do?

After a time delay, the acquired immune system finally sets itself in motion. It is different for every person and depends on what we have experienced and with which pathogens we have come into contact. While T cells help destroy infected cells, B cells form antibodies that can keep the virus in check. In the case of the coronavirus, these are neutralizing antibodies that bind to the spike protein of the virus. This is the site of attack of the virus, with which it enters the host, i.e. our human cell. Neutralizing antibodies specifically incapacitate the spike protein. Our immune system remembers the antibodies it has produced and is thus prepared for a new infection with the same intruder.

Is there an immunity? How long does it last?

The good news is that it is very likely there is an immunity. This is suggested by the proximity to other viruses, epidemiological data and animal experiments. Researchers infected four rhesus monkeys, a species close to humans, with SARS-CoV-2. The monkeys showed symptoms of COVID-19, the disease caused by the coronavirus, developed neutralizing antibodies and recovered after a few days. When the recovered animals were reinfected with the virus, they no longer developed any symptoms: They were immune.

Read more:What you need to know about the coronavirus

Rhesus monkey and humans share about 90% of their DNA

The bad news: It is not (yet) known how long the immunity will last. It depends on whether a patient has successfully developed neutralizing antibodies. Achim Hrauf estimates that the immunity should last at least one year. Within this year, every new contact with the virus acts as a kind of booster vaccination, which in turn might prolong the immunity.

"The virus is so new that nobody has a reasonable immune response," says the immunologist. He believes that lifelong immunity is unlikely. This "privilege" is reserved for viruses that remain in the body for a long time and give our immune system a virtually permanent opportunity to get to know it. Since the coronavirus is an RNA (and not a DNA) virus, it cannot permanently settle in the body, says Hrauf.

The Heidelberg immunologist Stefan Meuer predicts that the novel coronavirus will also mutate like all viruses. He assumes that this could be the case in 10 to 15 years: "At some point, the acquired immunity will no longer be of any use to us because then another coronavirus will return, against which the protection that has now been formed will not help us because the virus has changed in such a way that the antibodies are no longer responsible. And then no vaccination will help either."

How can we take advantage of the antibody response of the immune system?

Researchers are already collecting plasma from people who have successfully survived an infection with SARS-CoV-2 and are using it to treat a limited number of patients suffering from COVID-19. The underlying principle: passive immunization. The studies carried out to date have shown positive results, but they have usually been carried out on only a few people.

Read more:Coronavirus: How do ventilators work?

Research on antibodies is in high gear

At best, passive immunization is used only when the patient's own immune system has already started to work against the virus, says Achim Hrauf: "The longer you can leave the patients alone with the infection before you protect them with passive immunization, the better." Only through active immunization can one be protected in the long term. At the same time, it is difficult to recognize the right point in time.

PCR (polymerase chain reaction) tests are currently used to find out whether a person is infected with the coronavirus. With the help of PCR, it is not possible to tell whether or not there is reproducible viral RNA; it is just a proof of whether the virus is still present, dead or alive. A PCR test cannot tell us whether our immune system has already intervened, i.e. whether we have had contact with the virus in the past, have formed antibodies and are now protected. Researchers are therefore working on tests that check our blood for the presence of antibodies. They are already in use in Singapore, for example, and are nearing completion in the USA. With the help of these tests, it would finally be possible to gain an overview of the unclear case numbers. In addition, people who have developed antibodies against the virus could be used at the forefront of health care, for example. An "immunity passport" is even under discussion.

A PCR (polymerase chain reaction) laboratory

Is it possible to become infected and/or ill several times with the coronavirus?

"According to all we know, it is not possible with the same pathogen," says Achim Hrauf. It is possible to become infected with other coronaviruses or viruses from the SARS or MERS group if their spike proteins look different. "As far as the current epidemic is concerned, it can be assumed that people who have been through COVID-19 will not become ill from it for the time being and will not transmit the virus any further," he says.

How long before you're no longer contagious?

A study carried out on the first coronavirus patients in Germany showed that no viruses that are capable of replication can be found from day eight after the onset of symptoms, even though PCR can still detect up to 100,000 gene copies per sample. This could change the current quarantine recommendations in the future.

Medical assistants need protection when testing suspected coronavirus patients

According to the Robert Koch Institute, patients can currently be discharged from hospital if they show two negative PCR samples from the throat within 24 hours. If they have had a severe case of the disease, they should remain in domestic isolation for another two weeks. For each discharge, whether from hospital or home isolation, they should have been symptom-free for at least 48 hours.

Why do people react differently to the virus?

While some people get off with a mild cold, others are put on ventilators or even die of SARS-Cov-2. Especially people with pre-existing conditions and older people seem to be worst-affected by the virus. Why? This is the hottest question at the moment.

It will still take a very, very long time to understand the mechanistic, biological basis for why some people are so much more severely affected than others, virologist Angela Rasmussen told The Scientist. "The virus is important, but the host response is at least as important, if not more important," her colleague Stanley Perlman told the magazine.

Stefan Meuer sees a fundamental survival principle of nature in the different equipment and activity of our immune systems: "If we were all the same, one and the same virus could wipe out the entire human species at once. Due to the genetic range, it is quite normal that some people die from a viral disease while others do not even notice it. "

Achim Hrauf also suspects immunological variants that could be genetically determined. Since interstitial pneumonia is observed with the coronavirus, the focus is probably on an overreaction of the immune system. However, it is also possible that each person affected may have been loaded with a different dose of the virus, which in turn leads to different outcomes. And finally, it makes a difference how robust the body and lungs are: Competitive athletes simply have more lung volume than long-time smokers.

The immune system needs many different types of fuel. Fruit and vegetables provide them. Your diet should be healthy and colorful: Oranges, red peppers, green leafy vegetables and red cabbage provide a potpourri of vitamins, and are especially rich in natural vitamin C.

In order to ensure your immune system is top-top, make sure you have all the necessary immunizations. Adults often forget to refresh vaccinations they had when they were young. Check if you need booster shots for tetanus, diphtheria, whooping cough, polio, hepatitis, pneumococcus, meningitis, measles, mumps, rubella, the flu and others. Be sure to talk to your doctor!

Scientific studies suggest that regular muscle training (jogging, nordic or pole walking, taking a stroll), three times a week for 20 minutes can boost your defenses. But be careful: overdoing it can also drain your immune system.

Sufficient sleep doesn't just allow your body to recuperate. During the slow-wave sleep phase, neurotransmitters are released and the immune system springs into action.

Studies show that good spirits and a zest for life promote a strong immune system. Laughing and playing don't just provide for a better quality of life, they also boost the body's defenses.

Negative stress activates the release of adrenalin and cortisol. These hormones can paralyze the immune system. Sensible stress and time management allows the body to rest and replenish new energy. Selective relaxation exercises like meditation, autogenic training and yoga can significantly boost the immune system.

Taking walks in the fresh air gives you a change of temperature and exercise - both stimulate the body's defense systems. Mucous membranes also benefit from improved circulation and the increased humidity makes it easier to fight off attacks.

Studies have shown that burning up short chain sugars like fructose and glucose uses up many vitamins that are no longer available to the body.

Alternating hot and cold showers help regulate body heat and improve blood flow. An invigorating massage with a massage sponge or brush stimulates the immune system even more.

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The immune system's fight against the coronavirus - DW (English)

Its become an all-too-common variety of news story: Dead whales whose digestive systems are clogged with plastic. Increasing numbers of seabirds eating plastic, often with dire consequences. Ditto with turtles and fish.

Plastic ingestion by aquatic life is well documented. Less well known is the damage plastic does to the immune systems of fish.

There's very little research done on that, Patty Zwollo said. A lot of studies have focused on the larger pieces of plastics. I think the field is still trying to figure out where the microplastics are in different animals, including fish.

Zwollo is an immunologist, a professor in William & Marys Department of Biology. Immunologists study the bodys mechanism that provides resistance to disease. Her lab has discovered that just as whales swallow plastic thinking its food, some cellular components of the immune system in fish swallow bits of microplastic that they mistake for invading pathogens.

Zwollo compares the immune system to an army: Its a complex organization that has evolved to protect the body from invaders.

First, an army needs to be trained to recognize the enemy, she explained. And then when it's trained to do that, it has all kinds of different ways of fighting the enemy.

Her research focuses on the immune systems in salmon and trout and she further specializes in a specific category of soldier in the immune system army. Its known as the B cell, a specialized white blood cell commando.

When B cells recognize a pathogen or a toxin or whatever, they will bind to the invader, Zwollo said. Theyll start to make antibodies and then remove the pathogen from your body.

Once bits of plastic get small enough the size of a bacterium they can be mistaken for bacteria or viruses and ingested by certain cells in the immune system army. An immune cells act of ingesting a foreign body is known as phagocytosis. Those cells are called phagocytes.

And once the plastic gets inside of the cell, they cant be digested because theyre not organic. Theyre plastic, so the plastic stays inside the cell, Zwollo explained.

She says that lab studies have shown that if an immune cell absorbs a great deal of microplastic, the cell will die pretty quickly. But thats probably not biologically relevant, she added, explaining that in the natural environment, the levels of microplastic are almost certainly much lower than what the cells were getting in the lab.

So now that my students are feeding cells very small amounts of those microplastics, really low levels, she said. And then we see that they do survive longer, but they still die. So probably that is more realistic in comparison with what happens in the oceans.

When it comes to B cells, things get a little more complicated. B cells in mammals differ in a number of ways from B cells in fish, Zwollo explained. Its one of the many complexities in the study of the immune system. For one thing, mammals produce B cells in their bone marrow.

Fish dont have bone marrow, she said. So all their immune cells are made in this weird organ, the anterior kidney. The kidney of fish is very different from our kidney.

More to the point, mammalian B cells are not phagocytic they do their antibody work without engulfing the invading pathogen (or errant microsliver of plastic). Our B cells bind to the invader, then start producing antibodies.

But in fish, B cells can also be phagocytic, she said. So that, to me, is the most interesting thing about it. It doesnt seem to just affect phagocytes.

Zwollo stressed that her labs results are preliminary. She recently received funding from the National Oceanic and Atmospheric Administration to continue her studies on the effect microplastics are having on the immune systems of trout and salmon, commercially important fish.

After Zwollos lab completes its work, the second aspect will be conducted at William & Marys Virginia Institute of Marine Science, where researchers will expose whole fish to microplastics.

Ill be involved in that part too, she said. But most of my contribution will be in the first aspect.

She said she expects her investigations to take another year. Much of the work in the Zwollo lab is done by students. She has a graduate student, Fatima Quddos, working on the project. She also has an undergraduate, Lauren Abderhalden 22 involved.

Lauren is culturing cells, Zwollo said. Ive given her a lot of freedom, so she can learn the effect of little tiny plastic beads versus beads that are a little larger. What is the effect of concentration? And time, she is looking at how long you have to leave those cells with the microplastics.

Zwollo is teaching two sections of Immunology Laboratory this semester with eight students in each section. Shes launched her lab students loose on a journey of discovery.

I basically told them, all right, you get to decide what sizes of beads you want to work with, she said.

The lab students set their own course, deciding on all the conditions for their own experiments. Then, of course, they will analyze the data.

The students are really engaged, Zwollo said. Im interested in anything that comes out, pretty much. Because we really dont know much about this situation.

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Immune-system cells of fish are ingesting plasticand then dying - William & Mary News