StemCell Therapy

Reprinted with the kind permission of Cort Johnson and Health RisingMost people with chronic fatigues syndrome (ME/CFS) and fibromyalgia (FM) know the consequences of poor sleep the fatigue and pain, the difficulty concentrating, the irritability and more. Sleep is when our body rejuvenates itself; no sleep no rejuvenation. Given how important sleep is to our health, its no surprise that poor sleep is the first symptom many ME/CFS and FM doctors focus on.The effects of poor sleep go beyond just feeling bad, though. It turns out that poor sleep can have significant effects on our immune system effects, interestingly, which are similar to whats been found in the immune systems of people with ME/CFS and FM. Theres no evidence yet that ME/CFS and FM are sleep disorders that the problems ME/CFS and FM patients face are caused by poor sleep but depriving the body of sleep can cause one immunologically, at least, look like someone with these diseases.Why Sleep Is Important for Health: A Psychoneuroimmunology Perspective-Michael R. Irwin. Annu Rev Psychol. 2015 January 3; 66: 143172. doi:10.1146/annurev-psych-010213-115205.Irwin begins his review on sleep and immunology by noting the explosion in our understanding of the role sleep plays in health over the past decade. First, Irwin demolishes the idea that sleep studies are effective in diagnosing insomnia or sleep disturbances other than sleep apnea. Far more effective than a one or two-night sleep study is a home based sleep actigraph study which estimates sleep patterns and circadian rhythms over time and is coupled with a sleep diary.In fact, Irwin points out that the diagnosis of insomnia in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) is based solely on patient reports of difficulties going to sleep, maintaining sleep, having non-restorative sleep (common in ME/CFS) and problems with daytime functioning (fatigue, falling asleep, need to nap). (Problems with daytime functioning are actually required for an insomnia diagnosis.)Several effective sleep questionnaires exist including the Insomnia Severity Index, which assesses sleep quality, fatigue, psychological symptoms, and quality of life and the Pittsburgh Sleep Quality Index, a 19-item self-report questionnaire that evaluates seven clinically derived domains of sleep difficulties (i.e., quality, latency, duration, habitual efficiency, sleep disturbances, use of sleeping medications, and daytime dysfunction).Assess Your Sleep QualityThe Immune System and SleepThe immune system is vast and incredibly complex and has its own extensive set of regulatory factors, but is itself regulated by two other systems, the HPA axis and the sympathetic nervous system. Both are involved in the stress response and both are affected in ME/CFS and FM. One the HPA axis is blunted in ME/CFS, while the other the sympathetic nervous system is over-activated.Poor sleep, it turns out activates both system. The HPA axis is generally thought to be blunted, not activated, in the morning in ME/CFS patients, but the sympathetic nervous system (SNS), on the other hand, is whirring away at night (when it should be relaxing) in both FM and ME/CFS. (Having our fight or flight system acting up at night is probably not the best recipe for sleep.)Sympathetic nervous system activation, in fact, was the only factor in one Australian study which explained the poor sleep in ME/CFS. The authors of a recent FM/autonomic nervous system study went so far as to suggest that going to sleep with FM was equivalent to undergoing a stress test (!). Heart rates, muscle sympathetic nervous activation, and other evidence of an activated sympathetic nervous system response made sleep anything but restful for FM patients. In fact, the authors proposed sleep problems could be a heart of fibromyalgia.

Many questions have involved the roles pathogens play in ME/CFS and FM. Thats intriguing given the almost universally poor sleep found in the disorders and role recent studies indicate that sleep plays priming the immune systems pump to fight off invaders. During sleep, pathogen-fighting immune cells move to the lymph nodes where they search for evidence of pathogens. If pathogens are present, those immune cells mount a furious (and metabolically expensive) immune response.

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Is Poor Sleep Pummeling the Immune System in ME/CFS and Fibromyalgia? A Vicious Circle Examined - ProHealth

What most of us know about the canine immune system can fit into this paragraph. Their immune system protects them from infection and disease; when it fails, disease or an allergic reaction occur, pet food companies tell us their ingredients support the immune system.

If only it were that simple. There are two parts to the immune system. The default setting, if you will, is called the innate immune system. It consists of the skin, mucous, specialized cells in the saliva, stomach acid and certain cells in the body called phagocytes.

You might remember from your Conversational Greek classes that phago refers to eating. Phagocytes engulf foreign matter, and they arent too particular about what they engulf. Together, these elements make up the innate immune system; the bodys first line of defense.

As it often happens, repeated exposure to a substance will allow your body to build up a resistance to that substance. The innate immune system has nothing to do with that. But it does do a pretty good job at what it was designed for, which is defense.

The other half of this duo called the immune system is known as the adaptive immune system. Now thats a system. It defends against specific foreign invaders and, in its tool box, has a variety of tools that enable it to do battle.

If the invader simply needs a whack on the head to disable it, the adaptive immune system whips out its hammer. If it needs to cut off a germs legs to disable it, the system whips out its saw.

Not only does it recognize specific invaders and adapt to disable them, but it remembers them, too, so if they try to pull a fast one and attempt to get in again, the adaptive system responds with a swifter, more powerful tool.

The body can build up immunity to diseases in two ways. Active immunity is when the body is exposed to a substance either by natural means or by vaccination, and develops its own antibodies.

Passive immunity is achieved by receiving another animals antibodies. Examples of this would be the immunity received by the fetus from the placenta, from the colostrum consumed in the hours immediately following birth, or from bone marrow transplants.

But, alas, nothings perfect. Sometimes the immune system has a brain cramp, mistakenly recognizes a part of the body as the enemy, and goes on the attack. This is known as autoimmunity. The system can also overreact or it can fail to react at all.

If the immune system fails, it could mean that, just as in the old Wonder Ball song and game: The game for you is past, my friend, and you are out. Note to GenXers and subsequent generations: you might need to consult Prof. Google on that one, or ask Grammy or Grampy.

While the human and animal immune systems basically function in the same manner, theres still a lot that they dont know, especially with regards to animals.

Thats probably because funding for research in animal science is a lot harder to come by.

This lack of complete knowledge, though, has been cited as a major factor in the veterinary science communitys inability, thus far, to establish uniform immunization protocols. Vets, based on training and experience, still differ on the value and frequency of some immunizations.

Bob Bamberg has been selling pet products and writing about pets, livestock and wildlife for three decades. He can be reached at petsap@comcast.net.

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BAMBERG: The canine immune system - The Sun Chronicle

The effects of spaceflight on the human body have been studied actively since the mid-20th century and it is widely known that microgravity influences metabolism, heat regulation, heart rhythm, muscle tone, bone density, the respiration system.

Last year research from the US also found that astronauts who travelled into deep space on lunar missions were five times more likely to have died from cardiovascular disease than those who went into low orbit, or never left Earth.

Astronauts are fitter than the general population and have access to the best medical care, meaning that their health is usually better than the general population. Those of comparable age but who never flew, or only achieved low Earth orbit, had less than a one in 10 chance of death from cardiovascular disease.

But the chance of death rose to 43 per cent for those who reached the Moon or deep space, probably because of the impact of deadly space radiation.

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How our immune systems could stop humans reaching Mars - Telegraph.co.uk

Home Immune System Simple tips to boost your immune system

It may be hard to believe, but summer is coming to an end, which means fall is just around the corner. Fall brings with it colorful leaves, cooler temperatures, and unfortunately, cold and flu season. Instead of falling victim to illness this fall, try these simple tips to start boosting your immune system now so you can have a cold- and flu-free fall.

A big culprit of a weak immune system is exhaustion, both physical and mental. When we are exhausted, our immune system cant work its best to fight off germs that enter the body, which means you get sick. With all of lifes demands, it seems many of us are suffering from some type of exhaustion. Combatting it can improve your immune system. Ensuring you get a good nights sleep each and every night can help reduce exhaustion and also give your body the appropriate time to recover from the days stresses.

Other key areas that can help improve your immune system are food, exercise, hormones, and nutrition.

Food goes a long way in fueling exhaustion. Just think about it. If youve ever consumed a large meal, you probably felt like you needed a nap immediately after. Eating certain foods can go a long way in either promoting energy or fatigue. Steering clear of processed foods is a good step in promoting energy and improving your immune system. This means consuming foods like whole grains, fruits and vegetables, and lean meat. These foods will help ensure your body gets the adequate nutrition to boost the immune system rather than weigh it down.

Another tip is to eliminate trans fats and saturated fats, refined sugars, and empty carbohydrates, as these foods can make you feel sluggish along with contributing to other health conditions like obesity, blood pressure, and cholesterol.

There are specific foods, herbs, and spices that can work to boost the immune system too. These include garlic, radish, hot mustard, blueberries, and pomegranates.

Ensuring youre well hydrated also keeps you energized and flushes the body of toxins.

Lastly, eat foods that dont promote weight gain and watch your calories. Being overweight slows down your immune system, making it less effective at fighting bacteria and viruses.

Exercise is another great method to improve the immune system. This is because exercise supports all bodily functions such as improving heart health, bone health, and lung function, to name a few. When the inside of your body is working top-notch, your immune system will too.

Furthermore, regular exercise supports healthy blood circulation and good blood circulation supports immune cells.

If exercise isnt your thing, completing housework can also offer you similar benefits. Whether you are vacuuming, gardening, or even dusting, the goal is to complete an activity that gets your heart pumping and keeps you moving.

Boosting your immune system doesnt have to be complicated, and if you start now, then you can have an illness-free fall. Just adhering to some basic fundamentals of good sleep, proper nutrition and food, and regular exercise can help you boost your immune system.

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Simple tips to boost your immune system - Bel Marra Health

A new drug to fight cancer has just been approved in the United States.

The US Food and Drug Administration (FDA) has described its decision as historic.

They have approved a medicine called CAR-T - the first living drug for cancer - which can successfully treat a certain type of blood cancer in 83 per cent of people.

It works by redesigning the patients own immune system so it attacks acute lymphoblastic leukaemia.

White blood cells are extracted from the blood and then genetically reprogrammed to find and eliminate cancer.

They are then inserted back in the patient where they will then multiply.

Unlike current treatments, such as surgery or chemotherapy, the drug can be tailored to each individual.

The treatment - which will be marketed as Kymriah - has been created by Novartis who are charging $475,000 (approximately 367,000).

We're entering a new frontier in medical innovation with the ability to reprogram a patient's own cells to attack a deadly cancer, said Dr Scott Gottlieb, from the FDA.

New technologies such as gene and cell therapies hold out the potential to transform medicine and create an inflection point in our ability to treat and even cure many intractable illnesses."

Kymriah will be offered to patients when normal treatments fail.

Researchers treated 63 patients with CAR-T therapy.

Within three months 83 per cent of them were in complete remission.

However the therapy does come with some risks.

It can lead to potentially life-threatening cytokine release syndrome, but this can be controlled with drugs.

The treatment could also help tackle other types of blood-based cancers.

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Cancer treatment news: 'Historic' new drug could redesign immune system to FIGHT leukaemia - Express.co.uk

Credit: NYU School of Engineering

Gaining a better understanding of immune cells allows physicians to more effectively diagnose, monitor, and treat a wide range of diseases. Their complexity and sheer number make studying immune cells a difficult challenge, however.

Recently, researchers at the NYU Tandon School of Engineering, led by Assistant Professor of Mechanical and Aerospace Engineering Weiqiang Chen, were awarded a three-year grant from the National Science Foundation (NSF) to develop a new platform that combines an efficient microfluidic immune cell isolation technique and an ultra-sensitive nanoscale biosensor that will provide biologists and clinicians with a new approach to analyzing the proteins secreted from individual human immune cells.

Collaborating with co-principal investigator Pengyu Chen of Auburn University, and Assistant Professor of Endocrinology Jose O. Aleman and Pathologist Matija Snuderl of NYU's School of Medicine, Chen has devised a dual system that first separates a single immune cell from a microliter of blood (easily obtained with a simple pinprick) and then performs a multi-subset, multiplex functional immune analysismapping its phenotype, identifying its exact variety, and tracking its function.

"Current techniques look at a large number of cells and average the results, which doesn't permit for a truly granular examination," Chen explains. "In addition to conducting our analysis on a single-cell level, we're getting results about the immune status of patients in near real-timeallowing clinicians to test the efficacy of their therapies quickly enough to modify them if needed."

Not only will single-cell analysis allow medical personnel to modify their treatment in a timely enough way to significantly improve patient prognosis in cases of immune system disorders like HIV, sepsis, malaria, and tuberculosis, it may enable the deployment of personally tailored immunotherapy for certain diseases, such as glioblastoma, an aggressive form of cancer.

"We hope to help open new doors in the field of immunotherapy by making treatment more agile, responsive, and personalized," Chen says, "and to one day improve the outcome for countless patients."

Explore further: Researchers discover new immunotherapy combination effective at killing cancer cells

Provided by: NYU School of Engineering

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Understanding the immune system at the nanoscale - Medical Xpress

While much of the excitement around CRISPR gene editing focuses on its medical and public health applications, the ability to precisely edit virtually any DNA sequence is a revelation for basic research. In the latest demonstration, researchers at the University of California and elsewhere have used a modified version of CRISPR gene editing to identify genetic regulatory elements (enhancers) involved in autoimmune diseases.

The latest research, published this week in Nature, was led by Alexander Marson at the University of California San Francisco (UCSF) and Jacob Corn at the University of California Berkeley (UC Berkeley). The two researchers are also affiliated with the Innovative Genomics Institute (IGI), a joint UCSF-Berkeley initiative (Corn is cofounder and director), which aims to drive genome editing in medicine and agriculture.

Over the past few years, most studies utilizing CRISPR have employed a bacterial enzyme called Cas9 to engineer precise double-stranded cuts in a targeted stretch of DNA, usually in a gene. But there are many types of Cas (CRISPR-associated sequence) proteins that have different DNA cleavage and editing properties.

The new study used a method called CRISPR activation (CRISPRa), which uses a blunted version of a Cas enzyme that preserves the sequence-targeting properties but does not cleave the DNA. It was developed in 2013 by UCSF/Howard Hughes Medical Institute investigator Jonathan Weissman and colleagues. Weissman uses a musical analogy: while CRISPR/Cas9 can effectively repair a wonky key on the genomic keyboard, CRISPRa offers the possibility of composing a full score.

Using CRISPRa, Corn, Marson and colleagues have surveyed the human genome for regulatory regions called enhancersDNA motifs that can upregulate a gene sequence and may reside many thousands of bases away from the gene sequence itself. The IGI team focused on enhancers for a gene that affects the development of T cells, a key component of the immune system. Some of these enhancers are likely to have critical roles in the aberrant pattern of gene regulation that leads to autoimmune disorders such as Crohns disease and inflammatory bowel disease (IBD).

"Not only can we now find these regulatory regions, but we can do it so quickly and easily that it's mind-blowing," said Corn. "It would have taken years to find just one [enhancer] before, but now it takes a single person just a few months to find several."

Scientists can look for potential enhancer sequences based on how they interact with proteins that bind to DNA, but figuring out which enhancers work with which genes is much more challenging. Simply cutting out an enhancer with CRISPR/Cas9 doesn't help, because it won't have a noticeable effect if the enhancer is inactive in the particular cell type used in an experiment.

If you think of the genome as a model home with 22,000 lightbulbs (the genes) and hundreds of thousands of switches (the enhancers), the challenges have been finding all of the switches and figuring out which lightbulbs they control and when. Previously, CRISPR has been used to cut out wires looking for those that would cause a bulb to go dark, giving a good idea of what that section of the circuit was doing. However, cutting out a light switch when it's off doesn't tell you anything about what it controls. So, in order to find certain light switches, it has been common to try to mimic the complicated chemical cues that activate an enhancer.

But using this method, "you can quickly go insane trying to find an enhancer," said Benjamin Gowen, a postdoctoral fellow in Corn's lab at Berkeley and one of the study's lead authors.

A better approach would be a universal "on" switch that could target any part of the genome and, if that part included an enhancer, could activate that enhancer. Fortunately, CRISPRa, recently developed by Jonathan Weissman, Ph.D., professor of cellular and molecular pharmacology at UCSF and codirector of the IGI, is just such a tool. CRISPRa uses a "blunted" version of the DNA-cutting Cas9 protein, strapped to a chain of activating proteins. Although CRISPRa also uses guide RNA to target precise locations in the genome, instead of cutting DNA, CRISPRa can activate any enhancers in the area.

While the first applications of CRISPRa involved using a single guide RNA to find promoterssequences right next to genes that help turn them onthe UCSF/Berkeley team behind the new study realized that CRISPRa could help find enhancers too. By targeting the CRISPRa complex to thousands of different potential enhancer sites, they reasoned, they would be able to determine which had the ability to turn on a particular gene, even if that gene was far away from the enhancer on the chromosome.

"This is a fundamentally different way of looking at noncoding regulatory sequences," said Dimitre Simeonov, a Ph.D. student in Marson's lab at UCSF and the study's other lead author.

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CRISPR Genome Scan Reveals Key Immune System Regulators - Genetic Engineering & Biotechnology News (blog)

By combining new system-biological analyses and advanced data analysis, researchers at Karolinska Institutet have been able to monitor the maturation process of the immune system of leukaemia patients who have undergone stem cell transplantation. The technique, which reveals complex interactions between cells and proteins, can be used for other diseases to generate new knowledge about the regulation and dysregulation of the immune system, which can eventually give rise to new, improved immunological therapies. The study is published in Cell Reports.

Immunotherapy is a rapidly growing field in which the immune system of patients is manipulated in order to fight disease, and in which considerable progress in the treatment of cancer, above all, has been reported in recent time. One of the best-established and most effective immunological therapies is allogeneic stem cell transplantation for leukaemia, in which the patient's own diseased bone marrow is replaced by healthy donor material. In some patients, however, the grafted immune system fails to mature properly, which can cause serious infection, undesired attacks on healthy tissue or a cancer relapse.

Using advanced analytical tools, researchers at Karolinska Institutet have now studied the maturation process of the immune system in 26 leukaemia patients receiving treatment at Karolinska University Hospital. They monitored the patients for one year after completed stem cell transplantation and used mass cytometry to study the different cell types of the immune system and the ProSeek method for simultaneous protein analysis. The analyses were then combined with modern machine learning techniques for data analysis, which enabled the integration of all data and global analyses of the entire immune system in blood.

"Previously, research has focused heavily on individual components, but the immune system is incredibly complex, involving many specialised cell types, and we think the important thing is precisely the interaction between these cells," explains Petter Brodin, doctor and researcher at the Science for Life Laboratory (SciLifeLab) and Karolinska Institutet's Department of Medicine in Solna. "Although such dynamic processes have been difficult to study due to technical limitations, it's now possible thanks to breakthroughs in technology."

Dr Brodin has led the present study, which has been able to identify patterns that can be linked to clinical complications in the patients. The technique is also applicable to other diseases involving the immune system, such as autoimmune diseases, allergies and infections. It is hoped that more and larger studies of the dynamics and regulation of the immune system will provide new clues that open doors to new therapies and more individualised treatments.

"This study can be seen as the first example of how extensive analyses and advanced data analysis, a concept we call precision immunology, can help us understand the function and dysfunction of the immune system and make the outcome of other immunological therapies more predictable," he says.

Explore further: New tool demonstrates differences in human immune systems

More information: "Mass cytometry and topological data analysis reveal immune parameters associated with complications after allogeneic stem cell transplantation". Cell Reports, online 29 August 2017.

Journal reference: Cell Reports

Provided by: Karolinska Institutet

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Thorough analysis reveals immune system dynamics after ... - Medical Xpress

Since the 2015 Zika outbreak, scientists around the world have been focused on learning as much as they can about the devastating, previously obscure virus. They've learned a lot about how it's transmitted, how long it can stay in a host's system and that it can lead to devastating birth defects. But, there are still some major blind spots.

"Zika virus has been very well studied for congenital disease, but we still do not know exactly what happens right after [the] mosquito bite," saidDr. Jae Jung, professor of molecular microbiology and immunology at USC and lead author of a new study in Nature Microbiology that aims to solve the mystery.

It's been unclear what happens immediately after the virus enters the bloodstream, particularly of pregnant women, that allows it to propagate before infecting an unborn baby. As it turns out, the mechanism of how the virus spreads is eerily similar to that of HIV.

"We found that Zika virus specifically targets the white blood cells," said Dr. Jung.

Once the virus enters the bloodstream of a pregnant woman, it tricks the immune system, suppresses it and spreads quickly.

When a healthy, non-pregnant person is infected with a virus, the immune system kicks into high gear. White blood cells don their pith helmets and turn into so-called " M1 macrophages" that act like little soldiers, catching the virus and killing it. Separate white blood cells (M2 macrophages)then come along to calm their M1 cousins to return the immune system to its neutral mode.

However, when the Zika virus enters the body of a pregnant woman it takes advantage of her unique biology. The immune systems of pregnant women are already compromised. Their bodies have been flooded with the chill M2 macrophages, which tell the body's immune system to relax. This immunity suppression allows the unborn baby to survive.

But, the Zika virus is sneaky. Since a pregnant woman's body is already predisposed to creating the chill cells, it convinces her body to create even more. So, rather than attack the Zika virus, the compromised immune system allows it to propagate. The virus then spreads, eventually crosses the placental barrier and infects the fetus. As a result, babies can be born with a host of neurological birth defects, including microcephaly.

Dr. Jung's team studied both the African and Asian strains of the Zika virus, but found that the Asian strain, which is spreading across the Americas and Southeast Asia, had a more profound impact on the immune systems of pregnant women particularly during the first and second trimester. During the third, the impact wasn't nearly as pronounced.

"It is very important to understand how the virus behaves in order to develop treatments and also ways to prevent this from happening," said Dr. Karin Nielsen from UCLA and one of the authors of the study.

Dr. Jung's lab previously identified the proteins in the Zika virus that can cause microcephaly in infants.

There's still a lot left to figure out. For instance, Dr. Jung said that it's possible that Zika vaccines, some of which have been proven effective on non-pregnant people, might not be as effective for pregnant women as ethical limitations have prevented their participation in vaccine trials.

"The Zika virus research has just began," Dr. Jung said."We've only studied for two years so far. HIV has been studied over 30 years."

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The Zika virus undermines immune system - 89.3 KPCC

News / Published: 24 August 2017

Researchers have shown for the first time how leprosy bacteria damage nerves by infiltrating the immune cells that are meant to protect us.

Credit: Bruce Paton/Panos

The research found that leprosy hijacks the immune system, turning an important repair mechanism into one that causes potentially irreparable damage to nerve cells.

The researchers used zebrafish that had been genetically modified to make their myelin fluorescent green.

They injected Mycobacterium leprae bacteria close to the fishes' nerve cells. The bacteria settled on the nerve and developed doughnut-like bubbles of myelin that had separated from the myelin sheath.

When the researchers examined these bubbles more closely, they found that they were caused by M. leprae bacteria inside macrophages the immune cells that consume and destroy foreign bodies and unwanted material in our bodies.But, crucially, although the M. leprae was consumed by the macrophages it wasnt destroyed.

The team also demonstrated how the damage occurs a molecule known as PGL-1 that sits on the surface of M. leprae reprogrammes the macrophage, causing it to overproduce a potentially destructive form of nitric oxide that damages mitochondria.

The international team, in the UK and USA, was part-funded by Wellcome.

The research findings mean that leprosy may share common characteristics with conditions such as multiple sclerosis and Guillain-Barr syndrome.

The researchers say its too early to say whether their study will lead to new treatments. There are several drugs being tested that inhibit the production of nitric oxide, but lead author Professor Lalita Ramakrishnan, at the University of Cambridge, says the key may be to catch the disease at an early enough stage to prevent damage to the nerve cells.

Leprosy is a neglected tropical disease. Its difficult to work with in the lab because its highly adapted to humans. Previously, armadillos were the only animal modelthat could reproduce aspects of the disease. The zebrafish model means researchers can now study the pathogenesis of leprosy in much more detail.

Credit: Bruce Paton/Panos

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Leprosy turns immune system against itself - Wellcome Trust

Like an invader spotting a weakness in a castles defenses, Zika targets specific white blood cells in a pregnant womans immune system, enabling the virus to spread and increasing the chances of harm to unborn babies, according to a new study by researchers at the University of Southern Californias Keck School of Medicine.

Because pregnant women are more prone to immune suppression a natural occurrence that prevents the body from rejecting the fetus Zika exploits that weakness to infect and replicate, stifling a bodys natural defenses in a way that resembles HIV, the study authors said.

The mosquito-borne virus that emerged in Miami last year has been mostly absent in Florida this year, with fewer infections and no local cases as of Monday. The Florida Department of Health has reported a total of 151 Zika cases, with all but one a sexually acquired case in Pinellas County contracted by Floridians while traveling outside the country.

The USC study, published in the journal Nature Microbiology, is the first to report that Zika targets certain white blood cells and converts those cells into immune system suppressors.

Researchers tested African and Asian Zika strains by infecting blood samples taken from men and women, including some who were pregnant, and then analyzing them at peak infection. They found that Zika made a beeline for white blood cells that help fight infections.

The Asian Zika strain pushed those white blood cells to transform into a different type of cell that tells the immune system to stand down because the threat is over, according to the study. The false signal stifles the immune system, allowing Zika to replicate.

Pregnant women have higher levels of the immune-suppressing cells, researchers said, which provides an opening for the Asian Zika virus to do more damage.

Previous clinical studies have found that Zika infection during the first and second trimesters of pregnancy increases the chances of delivering a baby with a birth defect or other abnormality. USC researchers found that the Asian Zika virus also is more harmful during a womans first and second trimester.

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Zika targets pregnant women's immune system, almost like HIV, study says - Miami Herald

This photomicrograph reveals Mycobacterium tuberculosis bacteria using acid-fast Ziehl-Neelsen stain; Magnified 1000 X. The acid-fast stains depend on the ability of mycobacteria to retain dye when treated with mineral acid or an acid-alcohol solution such as the Ziehl-Neelsen, or the Kinyoun stains that are carbolfuchsin methods specific for M. tuberculosis. Credit: public domain

Scientists have unlocked a key element in understanding how human lungs fight tuberculosis (TB). They hope their research findings, which were published today in the international peer reviewed journal Immunity, will help pave the way towards new treatment approaches for TB, particularly in an era of increasing antibiotic resistance to TB.

Multi drug resistant TB is a global problem. These strains are resistant to several or most of the antibiotics used to treat TB. The need to find new strategies for treating TB, beyond antibiotics, is therefore critical and urgent.

Scientists at Trinity College Dublin and St James's Hospital in Ireland, working in a team with the University of Cambridge and University of Seattle, have identified a way that TB hijacks our immune cells in the early stages of infection to allow it to establish an infection in the lung.

Tuberculosis is the world's number one infectious killer, but half of infected persons clear the invading TB bacteria (known as mycobacteria) after inhaling it into their lungs. To date, it has not been understood how the immune system in the lungs manages to do this.

The lung contains a population of specialised immune cells, known as alveolar macrophages, which are the first responders to bacterial infections. These alveolar macrophages patrol the lung engulfing and destroying any bacteria they encounter along the way.

Using transparent zebra fish, the University of Cambridge and University of Seattle researchers tracked the mycobacteria in real time and identified which cells they infected at different stages of the disease. They found that the more virulent strains of mycobacteria are able to hijack the macrophage immune cells in the lung causing them to produce a protein that attracts white blood cells from the circulation. These white blood cells fuse with the macrophages and in turn become infected.

The Trinity team of Dr Senadh O'Leary, Senior Research Fellow, Professor Joseph Keane, Professor in Medicine at Trinity and Consultant Respiratory Physician at St James's Hospital, and Dr Mary O'Sullivan, Associate Research Lecturer, used donated lung macrophage samples from patients in St James's Hospital to study the response of the human immune system to TB in the early stages of infection. They found that human alveolar macrophages behave similarly to zebrafish macrophages producing the same protein that attracts white blood cells to the lung. Unlike the resident alveolar macrophages these white blood cells lack the ability to curb the growth of mycobacteria which results in uncontrolled bacterial growth and inflammation and in the spread of the infection.

Dr Senadh O' Leary said: "We are fascinated how TB bacteria virulence factors can corrupt this human lung immune cell which is ordinarily exceptionally good at clearing infection. It's very exciting to work with our Cambridge colleagues on this research which improves our understanding of how TB infection compromises immunity. We are in a unique position to address the important challenges for TB treatment as we work with the human lung model. This allows us to continue in our research to design novel ways to support the effective lung cell and prevent infections in exposed people."

The Trinity/St. James's team is funded by the Health Research Board and the Royal City of Dublin Hospital Trust, and are now hoping to identify drugs that will enable these immune cells to stop the infection in its tracksby killing the mycobacteria before they attract white blood cells to the lung.

Mairead O Driscoll, Interim Chief Executive at the Health Research Board congratulated the team: "Antidrug resistant TB is a global problem. We're delighted to be able to facilitate international collaboration to tackle this challenge. These findings represent a significant breakthrough in our understanding of how the bacteria avoids our immune system."

"Ireland is lucky to have such brilliant researchers, who are genuine world leaders in their fields. The Health Research Board is determined to continue to develop Ireland's health research capacity, so that we have the people, the facilities, and the support structures to produce more results like this."

Explore further: Tuberculosis bacterium may undermine immune regulation to drive disease progression

Journal reference: Immunity

Provided by: Trinity College Dublin

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Scientists discover how tuberculosis hijacks the immune system - Medical Xpress

Maintaining body weight isnt as simple as burning off all the calories eaten in a day. The brain plays an important role. It determines what you eat, how much and when. And the brains immune cells contribute, too, a new study in mice shows. Turning on these cells can make a fatty diet more fattening. Getting rid of those cells, known as microglia, can make the animals eat less and gain less weight.

These microglia caninflamea particular area of the brain. And in mice, this process could make the animals gain weight even when they werent eating a fatty diet.

I think its really neat, says Kate Ellacott, who was not involved in the study. This is the first time anyones shown if you change the way microglia can behave if you make them more inflammatory you can impact bodyweight. Ellacott is a neuroscientist, someone who studies the brain, at the University of Exeter in England.

The immune system is a collection of cells that can move throughout the body to help fight infection and damage. When a part of the body is stressed or injured, the hurt part sends out chemical distress calls. Those messages are like an alarm. They tell immune cells where to swoop inso that they can destroy damaged cells or gobble up germs.

Along the way, immune cells cause inflammation. This response can include redness and swelling. People often think of inflammation as a swollen knee or the redness surrounding a cut. Here, Ellacott points out, the immune system works to restore balance. The immune system tries to repair tissues and get back to normal, she explains.

But sometimes, inflammation sticks around for the long term, even when its not supposed to. Such chronic inflammation does not have to include redness. But it will cause harm. If you have a disease where inflammation never goes away, you can get damage to the tissue, she points out.

One condition where chronic inflammation occurs is obesity. Eating a high-fat diet for a while makes animals gain weight and activates their immune cells, says Joshua Thaler. Hes an endocrinologist (someone who studies the hormones in the body) and a neuroscientist. He works at the University of Washington in Seattle.There,his team performed the new study.

The brain is full of cells called neurons. But they arent alone. A variety of other cell types live there too, Thaler notes. For a while, scientists thought some of these cells, called glia (GLEE-ah), were just there to support neurons and to hold them together. (In fact, glia comes from the Greek word for glue.) But glia are far more than just brain glue. Some of them, called microglia, act as an immune army in the brain. They move into injured areas and can turn on inflammation when things go wrong.

Microglia cells, like the one shown here, can become activated by a high fat diet. Afterward, it can foster a state of chronic inflammation in the brain.

TimoninaIryna/istockphoto

Thalers team already had found that one brain area gets inflamed when mice eat a high-fat diet. Called the hypothalamus, this brain area helps to regulate how much mice and people eat. They even showed similar changes in the brains of people with obesity.

Could the microglia in the hypothalamus be the reason why? To find out, Thaler and his colleagues fed high-fat diets to more mice. Then they gave some of these mice a drug that killed off microglia. Without these immune cells, those mice gained less weight and ate less food. But losing their microglia had no effect on mice dining on low-fat chow.

The researchers wanted to make sure microglia were causing the inflammation that led to weight gain. So they deleted a gene a set of cellular instructions. Microglia use this gene to make their inflammatory signals. Thetreated mice gained less weight on a high-fat diet, just as in themice with no microglia at all.

If stopping inflammatory signals made mice gain less weight, more inflammation might have the opposite effect. Thalers group decided to test that idea. They worked with mice that were unable to make an important inflammation-fighting molecule. These mice developed inflammation in their brains. They also gained weight even when they werent on a high-fat diet! That confirmed that brain inflammation alone could contribute to obesity.

Thaler and his colleagues published their findings July 5 in the journal Cell Metabolism.

Calling in the immune cavalry

Microglia are full-time brain residents. Theyre always there, Ellacott says. These cells move to wherever the brain needs them.

When mice eat a high-fat diet, the hypothalamus recruits microglia. And these immune cells then call for backup. In the new study, some of those backup immune cells had come from a mouses bone marrow.

Usually, immune cells in the marrow cant reach the brain. Theres a barrier between the blood and the brain that stops them. That blood-brain barrier exists to keep potentially dangerous cells and other foreign substances from getting in.

Somehow, a high-fat diet let those marrow-based backup cells break into the brain.

Some scientists had seen immune cells getting into other organs after a high-fat diet, Thaler notes. But his group has now shown it also happens in the brain. I was not a believer that the [immune cells] were going to come marching into the brain, he recalls, so it was a bit of a surprise.

Scientists might someday be able to reduce inflammation by targeting the microglia, Ellacott says. If they can develop a drug that works this way in people, scientists might use it to treat all types of brain diseases linked with inflammation, not just obesity.

Microglia in the brain may contribute to weight gain, Thaler says. But clearly they arent the whole story. Turning off the microglia, or stopping them from sending inflammatory distress calls, causes mice to gain less weight. But in the end, those mice still became overweight. And while mice with brain inflammation gained weight on even a low-fat diet, he notes that they never got as fat as did the mice downing high-fat chow.

The brains immune system may be a part of the obesity story, Thaler says, but theres clearly more we need to learn.

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Brain's immune system can play role in weight gain - Science News for Students

Air pollution could increase the risk of infection by damaging the immune system, according to a study.

Scientists have demonstrated for the first time that nano-sized particles in traffic fumes reduce the body's ability to kill viruses and bacteria.

While the potential link between car-choked streets and illness has been the subject of much debate, the work at Edinburgh Napier University is the first to show this effect and presents significant human health implications.

Dr Peter Barlow, who led the research, said: "This is an area of research that is very poorly understood.

"We were extremely concerned when we found that air pollution particles could inhibit the activity of these molecules, which are absolutely essential in the fight against infection.

"In light of these findings, we urge that strong action plans are put in place to rapidly reduce particulate air pollution in our towns and cities."

The study focused on tiny molecules found in the immune systems of humans and animals, known as antimicrobial peptides, which increase in response to infection.

It found carbon particles could trigger changes in the molecules, potentially resulting in "an increased susceptibility to infection".

The implications are potentially profound for people living in areas of high air pollution, who breathe in huge concentrations of particles every day or absorb them through skin contact.

Those with pre-existing lung conditions like asthma or chronic obstructive pulmonary disease are said to be especially vulnerable.

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Traffic fumes 'increase infection risk by damaging immune system' - Birmingham Mail

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The Scripps Research Institute announced Thursday that it was awarded a five-year, $11.2 million federal grant to continue a long- running project to reveal the detailed workings of the mammalian immune system.

The project, which also includes professors from the Center for Infectious Disease Research in Seattle, Stanford University and the University of Texas Southwestern, aims to map the molecular and cellular interactions that underlie immunity and inflammation in health and disease. That in turn should enable the invention of better drugs and vaccines for infections, inflammatory diseases, and other immune-related ailments, according to TSRI.

The project has been funded by the National Institute for Allergic and Infectious Diseases, part of the National Institutes of Health, for 15 years.

It is one of the most productive large-scale science grants that NIAID funds, said Richard Ulevitch professor in TSRIs Department of Immunology.

The researchers use a system called forward genetics, in which the scientists create random DNA mutations in a population of test animals.

They screen the animals for resulting immune-related changes and, when they find significant ones, use state-of-the-art DNA sequencing technology to identify the mutated genes that caused the modifications.

The researchers also mine existing literature on gene and protein function, and apply the statistical and computational methods of systems biology, to connect the data points and thereby map the networks that underlie immunity.

Over the years, the scientists have published noteworthy findings in scientific journals and maintained online databases with their results.

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No parent likes seeing their child have injections. Yet, around 93% of parents across Australia protect their children against 15 serious diseases by giving them all the recommended vaccines on the National Immunisation Program Schedule. This success is due in part to the value of combination vaccines, which protect against two or more diseases in one go.

Combination vaccines mean kids need fewer injections overall. By adding several antigens (the part of the germ that stimulates the immune system) together in one vaccine, we can protect kids against up to six diseases in a few shots. These shots are typically given in a series of two or three injections over time.

Our new study released today in JAMA Pediatrics, backs the safety of a four-in-one combination vaccine designed to protect against measles, mumps, rubella and varicella (chickenpox) and known as the MMRV vaccine. We also show its added benefits in protecting kids by the time they reach pre-school.

Read more: Six myths about vaccination and why theyre wrong

Making a combination vaccine typically involves decades of research to ensure the precise balance of active components is included, the immune response to each component is effective, and even the slightest change in a vaccine doesnt change its safety profile.

This is stringently regulated across the world, by groups such as the Therapeutic Goods Administration in Australia and Food and Drug Administration in the USA, before a vaccine is even trialled in humans, or indeed ultimately licensed for use.

Once these combination vaccines are used, their safety (as well as the safety of other vaccines) is also actively monitored. One new way we do this in Australia is by monitoring any side-effects in real time. Parents respond to an SMS survey about their childs recent vaccination, the results of which are collated and posted online.

However, some parents question if giving an injection that protects against multiple diseases will overwhelm the immune system or be too much to handle. The answer is no for many reasons.

A review into parental concerns about combination vaccinations confirms the moment babies enter the world they are covered in millions of foreign germs. The infant immune system is no longer considered immature but is finely tuned to respond to the incredible number of viruses, bacteria and other things it meets early in life. Vaccines contain just a few antigens compared to what babies meet every day.

The researchers estimate that even if 11 vaccines were given to infants at one time, only about 0.1% of the immune system would be used up.

Read more: Explainer: how does the immune system work?

Rather than weaken the immune system, or putting it under strain, vaccines train the infant immune system to respond, without causing the terrible consequences of the disease itself. Combination vaccines do the same.

The design of vaccines has been increasingly tailored to leverage this unique biology, including the development of new combination vaccines.

Read more: Vaccine program changes protect kids, but with fewer ouches

For instance, in 2013, two new combination vaccines the MMRV vaccine and a combination vaccine against the Haemophilus influenzae type b and meningococcus type c bacteria (Hib-MenC) were added to Australias immunisation schedule, reducing the number of injections babies needed.

Our new study evaluated the impact of one these the MMRV vaccine since it was added to the schedule.

Before the MMRV vaccine was introduced, kids were protected against varicella (or chickenpox) with a separate vaccine. And they received their second dose of measles-mumps-rubella (MMR) vaccine at age four years, quite a big gap after their first-birthday dose of MMR.

By introducing this combination MMRV vaccine earlier (at 18 months), our study showed the second dose of vaccine against measles provided early comprehensive protection against this deadly disease.

While the first vaccine dose (given at 12 months) only gives a full immune response in about 90% of children, giving a second dose boosts immunity to more than 95% and also helps to provide longer lasting protection.

Our study showed not only that the percentage of children fully protected against all four diseases is now greater compared with when MMR was separated from the varicella vaccine, it is also occurring at a much earlier age.

On time vaccination (within 30 days of the recommended age) has now improved by 13.5% (from 58.9% to 72.4% of children). This means many more children are protected against measles, chickenpox, mumps and rubella (German measles) before entering pre-school.

Another important part of our evaluation was to ensure that introducing this vaccine was safe. If the combination MMRV vaccine is given as the very first dose of measles-containing vaccine in very young children, it causes more cases of fever and a small increase in febrile seizures (a common, usually benign, but frightening convulsion in children) compared with giving the vaccines separately.

Our study examined if using the MMRV shot in the Australian program as the second dose would be linked to an increase in febrile seizures. When we examined all children who came to paediatric hospitals across the country with a febrile convulsion, then looked at what vaccines they had received, we found no increase in febrile seizures associated with this second dose given at 18 months.

So introducing this combination vaccine in 2013, which has taken decades to develop, has:

Combination vaccines not only mean fewer visits to the doctor or nurse for injections, they can have other benefits, as well as being safe.

Our study highlights how much information is considered before making any change to the immunisation schedule to introduce combination vaccines, and importantly, how carefully changes to the schedule are monitored and evaluated.

While combination vaccines might introduce extra antigens to a childs immune system in one go, they are a tiny, tiny proportion of what children meet as they grow. Being vaccinated trains a childs immune system to withstand some of the biggest and baddest germs they will encounter.

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No, combination vaccines don't overwhelm kids' immune systems - The Conversation AU

An overview of the study 'Genetic Regulatory Effects Modified by Immune Activation Contribute to Autoimmune Disease Associations'. Credit: New York Genome Center

It is widely recognized that people respond differently to infections. This can partially be explained by genetics, shows a new study published today in Nature Communications by an international collaboration of researchers from Germany and the United States. The study, "Genetic Regulatory Effects Modified by Immune Activation Contribute to Autoimmune Disease Associations," maps genetic variants that affect how much gene expression changes in response to immune stimulus. The findings offer novel insights into the genetic contribution to varying immune responses among individuals and its consequences on immune-mediated diseases.

"Our defense mechanisms against microbial pathogens rely on white blood cells that are specialized to detect infection. Upon encounter of microbes, these cells trigger cellular defense programs via activating and repressing the expression of hundreds of genes," explained one of the senior authors of the study, Dr. Veit Hornung from the Ludwig-Maxmilians-Universitt in Munich and formerly from the University of Bonn. "We wanted to understand how genetic differences between individuals affect this cellular response to infection," added Dr. Johannes Schumacher from the University of Bonn, another senior author of the study.

The human immune system plays a central role in autoimmune and inflammatory diseases, cancer, metabolism and aging. The researchers discovered hundreds of genes where the response to immune stimulus depended on the genetic variants carried by the individual. "These genes include many of the well-known genes of the human immune system, demonstrating that genetic variation has an important role in how the human immune system works," noted Dr. Sarah Kim-Hellmuth, the lead author of the study, from the New York Genome Center, Columbia University, the Max Planck Institute in Munich and formerly from the University of Bonn. "While earlier studies have mapped some of these effects, this study is particularly comprehensive, with three stimuli and two time points analyzed."

The study captured genetic variants whose effects on gene regulation was different depending on the different infectious state of the cells. These included four associations to diseases such as cholesterol level and celiac disease. Furthermore, the researchers discovered a trend of genetic risk for autoimmune diseases such as lupus and celiac disease to be enriched for gene regulatory effects modified by the immune state. "This supports a paradigm where genetic disease risk is sometimes driven not by genetic variants causing constant cellular dysregulation, but by causing a failure to respond properly to environmental conditions such as infection," said co-senior author Dr. Tuuli Lappalainen, from the New York Genome Center and Columbia University.

The investigators collected blood from 134 volunteers and treated monocytes - a type of white blood cells - in the laboratory with three components that mimic infection with bacteria or a virus. They then analyzed how cells from different individuals respond to infection by measuring gene expression both during the early and late immune response. Integrating the gene expression profiles with genome-wide genetic data of each individual, they were able to map how genetic variants affect gene expression, and how this genetic effect changes with immune stimulus.

"It's been known for a long time that most diseases have both genetic and environmental risk factors. But it's actually more complicated than that because genes and environment interact. As demonstrated in our study, a genetic risk factor may manifest only in certain environments," explained Dr. Lappalainen. "We are still in early stages of understanding the interplay of genetics and environment, but our results indicate that this is a key component of human biology and disease. The molecular approach that we took in our study can be a particularly powerful way for researchers to delve deeper into this question."

The study's analyses of gene expression patterns in a population scale provide a highly robust and comprehensive dataset of innate immune responses and show wide variation among individuals exposed to diverse pathogens over multiple time points. The research identified population differences in immune response and demonstrated that immune response modifies genetic associations to disease. The research sheds light on the genomic elements underlying response to environmental stimuli, and the dynamics and evolution of immune response.

Explore further: Study describes key RNA epigenetic marker's role in immune system

More information: Sarah Kim-Hellmuth et al, Genetic regulatory effects modified by immune activation contribute to autoimmune disease associations, Nature Communications (2017). DOI: 10.1038/s41467-017-00366-1

Journal reference: Nature Communications

Provided by: New York Genome Center

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Genetic variants found to play key role in human immune system - Medical Xpress

In 1898, scientists in Uruguay noticed that some of their laboratory rabbits were dying from a mysterious illness, their skin riddled with tumors and weeping wounds. The researchers named the disease myxomatosis. They showed that it was caused by a new virus. And they argued that this myxoma virushighly lethal, specific to rabbits, and spread by mosquito biteswas exactly what the Australian government was looking for.

Europeans had introduced rabbits to Australia at the end of the 18th century, whereupon the fuzzy critters started breeding like, well, yknow. A century later, they had become a serious problem for both the nations wildlife and its farmers. Perhaps a disease could control the bunny blight?

In 1950, after some resistance and much cajoling, government scientists finally released myxoma-infected rabbits into the Murray Valley of southeastern Australia. That summer, the virus blazed brightly, but its spark appeared to peter out. Then, by years end, it rekindled into an almighty conflagration that swept through southern Australia, killing millions of rabbits. Thus, inadvertently, began one of the great experiments in natural selection, conducted on a continental scale, wrote Australian scientist Peter Kerr.

The myxoma virus quickly evolved. The strain that had initially been used was almost inescapably lethal, killing virtually every rabbit it infected. But virologist Frank Fenner discovered that, within a few years, this strain had been replaced with milder ones, which killed less rapidly and frequently.

These events provided an unprecedented view of how viruses evolve in the wild. Theyve also permeated into the popular consciousness, creating an intuitive sense that lethal viruses eventually evolve into milder forms, which are less likely to completely wipe out their hosts. But the notion that everythings heading toward a state of long-term co-existence and happiness is not always the case, says Andrew Read, an evolutionary biologist based at Pennsylvania State University. There are plenty of examples where the virus has got nastier over time.

And as it happens, myxoma is one such example. It went from exceptionally nasty to just nasty, and now has turned round and cranked up the nastiness again, Read says.

The virus was never entirely defanged. After its release in 1950, it went from killing more than 99 percent of rabbits to killing around 75 percent of them, or under 50 percent in some cases. In response, the rabbits evolved resistance, shrugging off strains that would once have finished them off. And that relaunched the arms race between myxoma and rabbits, prompting the virus to evolve its own countermeasures, which it still deploys today.

Read worked out how it responded by teaming up with Peter Kerr, who had collected and stored myxoma samples from the last several decades. By exposing lab rabbits to these archived strains, the team showed that by the 1990s, the virus had gained a new ability: It could completely shut down a rabbits immune system. This stops the animals from effectively clearing the virus. Inadvertently, it also means the bacteria that normally live peacefully in the rabbits bodies run amok, spreading through their internal organs and causing septic shock. These rabbits never develop the skin tumors or any of the classic symptoms of myxomatosis. Instead, they die from massive and sudden infections. Their lungs fill with fluid and they start bleeding uncontrollably.

These immune-suppressing strains might have emerged as early as the 1970s, and theyre circulating broadly now. Still, their effects are hard to spot in wild rabbits, which still die from the same kinds of symptoms as they used to. Thats because their genetic resistance partly counteracts the viruss new ability, which only becomes clear when it infects lab animals that have no history of coevolving with this virus. The wild rabbits started to resist the virus, the virus started to kill them in a new way, and neither side gained any ground. Its like a duck in a stream, paddling like crazy under the water and not getting anywhere, says Read.

Laboratory experiments using bacteria and their viruses have shown that when hosts evolve resistance against infections, viruses can rapidly overcome host immunity, says Lotta-Riina Sundberg, from the University of Jyvskyl. But monitoring these long-term coevolutionary arms races in natural settings with such accuracy is challenging. Thats why the myxoma story is so important, she adds.

The same dynamics played out in Europe, where a different strain of myxoma was used to control rabbits, following the Australian success. There, too, the virus evolved into milder forms. And there, too, new immunosuppressive strains have emerged. No one knows what will happen in the future. In South America, myxomas birthplace, the virus causes an innocuous disease in the local cottontails. But theres no indication that the Australian or European strains are heading in that direction.

The broad lesson is that theres a variety of evolutionary trajectories that pathogens can take, says Read. There are situations, no question, where virulence can go quite low. Sexually transmitted diseases, for example, require hosts to be sexually active and that requires that they stay alive for some time. But theres no reason to think that the average long-term state will be coexistence, and thats a mistake thats permeated the public.

Consider rabbit hemorrhagic diseaseanother infection that Australia considered as a way of controlling rabbits, and that escaped from a quarantine facility in 1995. The virus behind the disease is transmitted by corpse flies, which are attracted to cadavers, so this virus actually benefits by killing its hosts in spectacular fashion. Its present in huge numbers at the time of death. As such, it started off lethal and has only become more so with time. In the United States, West Nile virus has become more virulent in house sparrows, in response to the birds evolving resistance. And Mareks diseasean illness of fowlbecame fouler after farmers treated birds with a leaky vaccine, which stops them from developing the disease, but not from becoming infected or spreading the virus.

These consequences are relevant to various companies and researchers who are trying to make farmed animals more resistant to diseases. Some are doing it by traditional breeding. Others are looking to genetic engineering. Whatever the route, the myxoma example shows that such measures could drive the evolution of more potent viruses. These may not be a problem for the resistant animals, just as immunosuppressive myxoma strains arent especially deadly to wild rabbits. But if the viruses spread to naive animals, they would suffer.

If you had a bunch of companies in one river system, and one is creating more resistant fish, causing pathogens to become more virulent, what does that do to the wildlife and the fish belonging to other companies? says Read. You have to ask about the long-term consequences. Maybe there are some types of resistance that are less likely to provoke this arms race than others. We need to understand that.

Read more:
The Next Chapter in a Viral Arms Race - The Atlantic

With Australia in the midst of what is likely to become its worst flu season in 15 years you can consider yourself lucky if you havent been hit yet.

Over 70,000 people have been struck down so far this year, but with many of us skipping a visit to the doctor the number is likely to be much higher.

Some of the confirmed cases were people that fell ill despite the flu vaccination. So we thought wed look at some other ways you can strengthen your immune system naturally including things we can do and eat.

There have been over 70,000 confirmed cases so far. Photo: Getty

With pregnant women, young children, and senior citizens most at risk, leading naturopath and sports nutritionist, Kira Sutherland, shared her three food immune boosters with Be.

AntioxidantsAntioxidants are nutrients within foods that are supportive to a strong immune system. Berries are packed with antioxidants, are low in sugar, and usually contain lots of fibre, Kira tells Be. Blueberries, for example, contain both vitamin C and K, and resveratrol, which is a fabulous antioxidant.

Kira also suggests juice, such as H2melon. Watermelon is high in water and lower in sugar than most regular juices, and contains vitamin C, lycopene, and beta-carotene, which are all antioxidants that help to support the immune system.

Berries are high in antioxidants and can strengthen the immune system. Photo: Getty

ProbioticsAccording to research, the digestive system represents almost 70 per cent of the entire immune system. Yoghurts contain great gut bacteria known as probiotics which are important for good digestive and gut health, Kira says.

RELATED: Sick man, 29, 'told by doctor he had flu' one day before he diedRELATED: Matt De Groot: What women don't realise about man flu

ProteinProtein is important for stabilising blood sugar levels and our immune systems depend on good quality protein to keep it working properly. Kira says many people will use protein powders to easily get their protein hit. Other good sources of protein include meat, fish, chicken, eggs, dairy, beans, soy foods, nuts and seeds.

Pregnant women, young children and elderly are most at risk. Photo: Getty

In terms of things you can do, Brisbane natural health expert Jo Formosa shares a few tips to ward off the flu.

Avoid rapid changes in temperature: The biggest one is going from warm to cold these dramatic changes impact how our system recovers.

Eat smaller meals: When youre sick you dont need to eat as much.

Avoid dairy products when you have the flu: This contributes to mucous and phlegm production, instead go for ginger and turmeric - in juice, milk or honey.

Jo says to avoid dairy when fighting the flu. Photo: Getty

Eat more warm soups: in particular with garlic, ginger and black pepper as this breaks up mucous and phlegm.

Stay warm when out in the elements: Even if it's sunny outside, its important to take care to keep the head and neck warm.

Stay warm. Photo: Getty

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Flu epidemic: How to boost your immune system naturally - Yahoo7 Be

In an evolutionary arms race with its host rabbits, the virus has evolved the deadly ability to suppress the rabbit's immune system. Credit: Kansas State University

In a classic example of the evolutionary arms race between a host and a pathogen, the myxoma virusintroduced to control the rabbit population in Australia in 1950has developed a novel and deadly ability to suppress the immune response of its host rabbits. New research shows that viruses collected in the 1990s are much more effective at shutting down the immune systems of rabbits that have never been exposed to the virus than are viruses from the 1950s.

"When a host develops resistance to a virus, the virus will often evolve ways to evade the host's immune response," said Andrew Read, Evan Pugh Professor of Biology and Entomology and Eberly Professor of Biotechnology at Penn State and an author of the study. "Instead of hiding from the rabbit's immune response, the myxoma virus has evolved ways to directly suppress it, leading to the development of a virus that is even more deadly to non-resistant rabbits."

A paper describing the new study appears the week of August 14, 2017, in the journal Proceedings of the National Academy of Sciences. The research suggests that efforts to artificially increase resistance to a virus through selective breeding, genetic engineering, or immunizationunless they completely prevent transmission of the viruscould accelerate the arms race, producing even more virulent viruses.

Wild European rabbits were introduced to Australia in the 19th century and quickly spread, wreaking havoc on the land and devastating crops. The myxoma virus was initially extremely effective in reducing the population of these invaders. The strain of virus that was introduced developed in a different species of rabbit in South America. Scientists at the time were interested in understanding how the virus would evolve in this new, European, host.

"This system has been studied since the 1950s as a classic example of an evolutionary arms race," said Peter Kerr of the University of Sydney, Australia and lead author of the paper. "The rabbits evolved resistance, the virus evolved ways to combat that resistance, and this continued in a back-and-forth, ever escalating way. We wanted to know how that arms race has continued since it was last studied in the early 1980s."

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The research team compared viruses collected in the 1990s to the original strain introduced to Australia in 1950. "We can compare how nasty a virus is in what we call a 'common garden'," said Read. "In this case, laboratory rabbits that have not been exposed to myxoma virus provide that common gardenthey have not developed resistance to mxyomatosis so we can compare how they respond to viruses from different eras."

Many of the viruses from the 1990s were extremely virulent, but the laboratory rabbits infected with them did not develop the usual symptoms associated with myxoma infection, including skin lesions and high fever. Instead, these rabbits developed a profound immune system depression, leading to massive bacterial infection and acute collapse syndrome, similar to sepsis.

"The rabbits infected with virus from the 1990s did not have a typical inflammatory response to the infection or develop fevers," said Isabella Cattadori, associate professor of biology at Penn State and an author of the paper. "This is further evidence that the virus is severely suppressing the immune response in these rabbits. The evolutionary arms race has produced a virus that instead of trying to evade the host's immune response, directly attacks it."

Although the original strain of myxoma virus introduced to Australia in the 1950s had some ability to suppress its host's immune system, this ability has increased over time and the acute collapse syndrome that it causes developed sometime after the studies in the 1980s.

"Our study shows that the evolutionary arms race between an infectious agent and its host's immune system can continue to escalate to produce new more dangerous viruses," said Read. "We need to be aware of this in areas like agriculture, and even human vaccinations, where we are artificially enhancing resistance. If our methods do not completely prevent transmission of the viruses we could be accelerating the evolution of more deadly viruses."

Explore further: A real Peter Rabbit tale: Biologists find key to myxoma virus / rabbit coevolution

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Viruses up their game in arms race with immune system - Phys.Org