StemCell Therapy

Magnetude Jewelry Fall 2020

MT AIRY, Md. (PRWEB) September 01, 2020

In a fall like no other, Magnetude Jewelry finds itself with the right product at the right time. Interchangeable fashion jewelry pendants and necklaces that allow one to change the stone based on mood and occasion is already a hot fashion trend, but in a year where everybody is looking for strategies to boost and improve the immune system, Magnetudes second key ingredient is about what the products are made of: Neodymium magnets.

Most people dont realize that their electrical energy is diminished by EMFs and can decrease their immunity, explains Magnetude co-founder Dr. Tracey Diner, DC. Wearing Magnetude Jewelry along with other healthy regiments like vitamins, good diet, and exercise, help us build up a stronger resistance to viruses and germs.

EMFs come from many sources in this high-tech age, including cell phones, Wifi, cell towers, and other electronic activity. Dr. Diner, a wellness doctor, and her partner Candice Loren, a noted artist and jewelry designer, started this company to pursue their joint passions for unique design and better health.

Magnetude Jewelry incorporates the most powerful healthy Neodymium magnets, energy elements of infrared, negative ion, and germanium in all of their interchangeable necklaces, bracelets, and earrings. These energy frequencies help to replenish the cellular function that EMFs destroy. With the fall flu season about to start and the expected second wave of COVID-19 on the horizon, innovative ways to stay healthier are at a premium.

Magnetude Jewelry should be worn all the time, so it has been designed with thousands of combinations to match any clothing the wearer chooses. There are product lines for men and pets, and this month Dr. Diner says she is launching a childrens line because children are at higher risk from EMFs, absorbing up to 10 times that of adults.

For further information about Magnetude Jewelry and the science behind it, visit http://www.MagnetudeJewelry.com.

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FALL 2020 - Magnetude Jewelry Fashion Line Supports the Immune System - PR Web

Wells: Is there any downside of giving people plasma, even if you dont know if its going to be specifically helpful to them?

Hamblin: There theoretically shouldnt be, but there could, and that is the reason that you dont just authorize these things, that you have an FDA to make sure that something is safe and effective ...

Kola: It seems like people have antibodies within three months of them having COVID-19. And I definitely had antibodies back in May when I was given an antibody test, but then, given the news out of Hong Kong, it looks like those antibodies might wane over time? When I imagine the plasma, am I imagining blood that has actual antibodies in it, or does it have the memory of how to make antibodies? Whats actually in the plasma?

Hamblin: Thats a great question Youre just getting the antibodies themselves. The act of producing them will involve the white blood cells that should be taken out of plasma

Wells: Theyre the things that make the antibodies ... and that do have the memory of how to make them?

Hamblin: Right When you transmit plasma, youre not teaching someone to make antibodies. Thats what happens by exposing them to the virus. Thats vaccination. Its called passive immunization, where you temporarily have these antibodies until your blood clears them out. Theyre gone, and youd theoretically have to get another transfusion.

Kola: So there would be the possibility that, having had COVID-19 in March, and maybe being called upon to donate plasma in October, my blood might not have the antibodies anymore that it had in May.

Hamblin: Yeah, that remains possible.

Kola: Wow.

Wells: Is that upsetting?

Kola: I think its like much to do with COVID: Just one of the sort of confusing complexities of it is that I know that I had the antibodies at one point. I cant know for sure that I have them now without another antibody test. And being someone who had it relatively early, my experience of the virus is myself and everyone around me learning about it almost in real time ...

Hamblin: Well, if it helps reassureI guess Katherine can explain the immunology here, because we had a whole episode on thisbut there is more to your bodys memory than just the presence of antibodies themselves. There are immune-messaging pathways such that even if you lost your antibodies, its possible that your body might be able to kind of quickly make new ones and call them back and have other ways of fighting off this virus so that, if you are reinfected, it is not so bad, even if you dont actively have the antibodies.

Kola: Can you explain how people like me who had COVID-19 and are hopeful about immunity should interpret the information from Hong Kong, because that was obviously, on the face of it, quite scary for people whove had an experience of COVID that they wouldnt wish to go through again.

Here is the original post:
Listen: Plasma and Immunity - The Atlantic

A new test that provides information on the immune response to the novel coronavirus in patients who need to take immunosuppressive drugs has shown that these patients can achieve a good immune response to SARS-CoV-2 despite immunosuppression.

A research team from the University Hospital at Ruhr-Universitt Bochum (RUB Bochum, Germany) has developed the test which can be used to adapt immunosuppressive therapy individually during a COVID-19 infection, such as following an organ transplantation. The test is of great clinical relevance for transplant patients as it provides information that goes far beyond a pure antibody test.

Transplant patients are affected in several ways: in addition to the chronic illness that led to organ failure and subsequent transplantation, transplant patients need to take medications that suppress the defenses of their own immune system. Chronically ill patients with impaired immune defenses have an increased risk of suffering from a severe COVID-19 infection. It was previously unknown whether patients could develop a sufficient reaction against the new coronavirus under the influence of immunosuppressive drugs.

With the help of the test, the team demonstrated that transplant patients are very capable of achieving a good immune response despite immunosuppression. In addition to high antibody titres, large quantities of T lymphocytes, which are responsible for killing infected cells, were found in the current case study.

Until now, it has not been known whether our transplant patients are capable of forming a sufficient immune response to the new coronavirus, said Professor Timm Westhoff, Director of Medical Clinic I at Marien Hospital Herne, who led the team of researchers. The data obtained help us to deal with immunosuppression during the current pandemic. The test allows us to individually adjust immunosuppression when a patient is suffering from COVID-19.

Related Links:Ruhr-Universitt Bochum

Read more from the original source:
New COVID-19 Test Shows Patients with Suppressed Immune Systems Can Also Achieve Good Immune Response to SARS-CoV-2 - HospiMedica

How do you strengthen the immune system, the bodys natural defense against disease and infections, is a very common question. The answers often include regular exercise, an adequate amount of sleep, no smoking or excessive alcohol drinking, and of course, a healthy diet.

However, some of these are probably hard to implement during a pandemic. Stress levels are high and most people are simply trying to manage each day as best as they can. Spending a lot of time planning meals that have all food groups is practically impossible, so individual items that have copious amounts of vitamins, minerals, and antioxidants all in one may come in handy.

24/7 Tempo used the U.S. Department of Agriculture site to determine fall foods, and consulted a clinical nutritionist to identify the best fall superfoods that may help boost immunity.

Eating the right foods is not rocket science, and superfoods is not a scientific term. Its a marketing term used to describe foods that are nutritionally dense, although often there are also misconceptions about which fruits and vegetables fit that description. Not all foods are created equal, and you only think some foods are healthy when, in reality, they wreak havoc on your body.

See the rest here:
29 Fall Superfoods That Will Boost Your Immune System - MSN Money

The coronavirus that causes COVID-19 has one major advantage over us it is a new human virus. Most people have not encountered the virus before, meaning their immune system is not primed and ready to fight it. When someone gets sick with COVID-19, there is a lag in an efficient immune response, giving the virus time to do significant damage before the immune system can reign in the infection.

It essentially becomes a race between how fast your immune system can clear the virus and how quickly the virus can replicate and induce damage, Agustin Melian, MD, Chief Medical Officer and Head of Global Medical Sciences at AlloVir, told BioSpace.

To develop an effective treatment or vaccine for COVID-19, scientists must understand how the immune system is impacted during the disease. One type of immune cell that is particularly important in the bodys response to COVID-19 is T-cells. T-cells perform many functions, including recognizing invading viruses such as the coronavirus that causes COVID-19.

Multiple studies from Wuhan, China reported that COVID-19 patients had very low T-cell counts; the sicker the patient, the lower their T-cell count. Lower T-cell counts were correlated with poorer outcomes (including higher risk of death) and T-cells isolated from COVID-19 patients also showed signs of exhaustion.

The elderly, patients with low T-cell numbers, and patients who express exhaustion markers on their T-cells are high risk groups in which nave cell responses (responses against a virus they have never seen before) may be deficient or delayed, thus allowing the virus to induce a large amount of damage, Dr. Melian explained. These patients may, therefore, benefit from AlloVirs approach which is designed to restore natural T-cell immunity in high risk patients.

Could giving high-risk COVID-19 patients functional T-cells against the coronavirus boost their immune system and help them recover? This is the question AlloVir aims to answer.

AlloVir creates allogeneic (off-the-shelf) virus-specific T-cells designed to treat common and devastating viral-associated diseases in vulnerable patients, such as those who are immunocompromised or patients who received an organ or stem cell transplant. Now, they are expanding their anti-viral T-cell arsenal and taking aim at COVID-19.

We believe AlloVirs technology is well positioned to treat patients with COVID-19 because our technology is designed to provide SARS-CoV-2 specific T-cell immunity while leaving non-infected cells intact, Dr. Melian commented. Our virus-specific T-cell candidates have been used to treat more than 275 immunocompromised patients with life-threatening viral infections and diseases and we believe it our approach may also have promise in treating COVID-19.

Fighting viruses with T-cells in immunocompromised patients

When you get infected with a virus, your immune system responds to the foreign threat by making specific T-cells that can recognize the virus. These specific T-cells prompt your immune system to destroy any cells infected by the virus.

However, if you have a T-cell deficiency, your immune system cannot robustly protect you. This is a major problem because an otherwise innocuous virus can become a serious infection, causing complications, and possibly even be life-threatening.

That is where AlloVir comes in. They address the underlying problem the weakened immune system. A weakened immune system can be beefed up by giving patients with T-cell deficiencies off-the-shelf virus-specific T-cells (VSTs) originally taken from healthy people. This restores their natural T-cell immunity and helps their immune system fight off the viruses.

At AlloVir, we are a leading innovator in discovering and developing allogeneic, virus-specific T-cell immunotherapies, Dr. Melian said. We are now excited to be applying our capabilities in discovering and developing SARS-CoV-2 specific T-cells to join the fight in developing a COVID-19 program for patients at high risk of severe and devastating disease.

AlloVirs virus-specific T-cell platform

To create AlloVirs T-cell therapies, the target virus is first studied carefully to identify its specific antigens (unique molecules on the outside of each virus that are specific to the virus and alert the immune system). The best antigens those that induce a strong T-cell response are used to create the therapy.

Next, blood is taken from healthy donors who have been exposed to the virus of interest and T-cells are isolated from the blood. The T-cells are activated in the lab they are trained to recognize the identified viral antigens, enabling the T-cells to selectively recognize only the desired virus.

After the T-cells have learned to recognize the specific virus, they are expanded to generate multitudes of cells. Once the activated, specific T-cells are created, they can be cryopreserved and kept for a long time, making them readily available as soon as a patient needs them. The entire process, from antigen selection to donor to ready-to-go T-cell treatment, can be completed in a matter of weeks. This process can be seen in the visual below.

Source: AlloVir

Patients are matched using the companys proprietary human leukocyte antigen (HLA)-matching formula. HLAs are proteins on the surface of cells that regulate the immune system.

Our proprietary donor selection algorithm, known as Cytokin enables us to cover >95 percent of patients in our target population from cells derived from a small number of donors, Dr. Melian said. This proprietary process of prospectively manufacturing cells for off-the-shelf use enables us to study our allogeneic cell therapies in large numbers of patients that suffer from global health crises, like seasonal influenza and, as we are discussing, the COVID-19 pandemic.

These T-cells are advantageous because they are active against a single virus or multiple viruses, are not patient-specific (so they are readily available) and are a single treatment that provides lasting protection. The biggest bonus is the immediate off-the-shelf use for time-sensitive infections in vulnerable populations, added Dr. Melian.

In addition to developing their COVID-19 therapy (called ALVR109), AlloVir has two other multi-virus specific T-cell therapies in development: Viralym-M (ALVR105) and ALVR106. Both therapies focus on treating viral diseases common to stem cell and solid organ transplant patients and other vulnerable populations.

Viralym-M targets six common viruses: BK virus (BKV), cytomegalovirus (CMV), adenovirus (AdV), Epstein-Barr virus (EBV, also called human herpesvirus 4), human herpesvirus 6, and JC virus (also called human polyomavirus 2). Although these viruses are widespread and infect most people, they only cause severe problems in people with weakened immune systems due to age, organ or stem cell transplant, or disease (such as diabetes or AIDS). In a Phase 2 study, 93 percent of 38 allogeneic stem cell transplant patients had a clinical response to Viralym-M treatment and functional Viralym-M cells lasted up to 12 weeks in the patients.

ALVR106 targets four common respiratory viruses: influenza, parainfluenza virus, respiratory syncytial virus (RSV), and human meta-pneumovirus (HMPV). While these viruses tend to cause mild to moderate respiratory illnesses, they can cause severe, life-threatening illness, especially in people with weakened immune systems. ALVR106 is still in preclinical development but clinical trials are expected to begin this year. Overall, AlloVir expects to have three new proof-of-concept (POC) Phase 1b/2 and three pivotal Phase 3 studies started over the next 6-18 months.

Off-the-shelf T-cells against COVID-19

While AlloVir originally designed their T-cell therapies for transplant patients, their platform can potentially be applied to any virus to create virus-specific T-cells. This versatility allowed AlloVir to pivot and create T-cells against SARS-CoV-2, the virus that causes COVID-19. This new investigational therapy, called ALVR109, is being developed as a stand-alone treatment, though it may also be incorporated into their ALVR106 respiratory virus therapy at some point in the future.

Normally, the body would make virus-specific T-cells on their own and these would clear the virus, commented Dr. Melian. We enable that process in patients who otherwise would be T-cell deficient to restore T-cell immunity by giving ex vivo expanded cells that come from patients who already have demonstrated a potent immune response and have cleared the infection.

The process of creating coronavirus-specific T-cells is the same as creating their other virus-specific T-cell therapies. First, blood is taken from people who have recovered from COVID-19 and the T-cells are isolated. Then, the cells are stimulated with viral antigens in the lab, expanded, and cryopreserved.

We purposely choose a broad range of viral antigens to stimulate the T-cells to ensure the virus cant circumvent the virus-specific T-cell therapy by mutating or developing resistance, Dr. Melian said. Working with a wide spectrum of viral activity is different than other approaches that just focus on one viral antigen.

An open-label Phase 1 trial (called BAT IT) is anticipated to start within the next few months. Initial clinical studies of ALVR109 aim to treat high-risk COVID-19 patients, such as the elderly, to prevent organ damage. Prophylaxis studies, where the T-cells could be given to high-risk or immunocompromised patients who are not currently sick with COVID-19, may be considered later.

Coronavirus-specific T-cells vs. COVID-19 convalescent plasma

You may be wondering if another treatment that uses blood from COVID-19 survivors, called convalescent plasma therapy, is similar to AlloVirs T-cell therapy. In convalescent plasma treatment, antibodies from COVID-19 survivors are isolated from their blood by separating out their plasma (the liquid part of the blood). The plasma is given to COVID-19 patients to help their immune system fight off the infection.

Although convalescent plasma and AlloVirs coronavirus-specific T-cell treatments are both derived from COVID-19 survivors blood, the two treatments are fundamentally different.

Antibodies and T-cells work in different areas of the immune system, explained Dr. Melian. Antibodies can go after viruses in circulating blood but cant necessarily see viruses in infected cells. On the other hand, T-cells are pleotropic and directly attack virally infected cells, turning off the viral factories. T-cells are interesting because it is a live therapy they can home to virally-infected cells and direct the immune system.

Dr. Melian went on to explain that T-cell approach may be more comprehensive because they can support other immune cells that work against viruses, such as B-cells that make viral-specific antibodies. T-cells can also stimulate cytokines including interferon (a group of signaling proteins the immune system uses to respond to viruses), which further activates the bodys antiviral response.

Providing virus-specific antibodies may be beneficial and protective for some viral infections, Dr. Melian added. We dont know how these antibodies affect COVID-19 patients yet, but COVID-19 has a high mortality rate despite standard of care treatment. In this respect, it is important that all viable approaches to treatment be evaluated and I am very pleased to see these therapies have entered clinical testing.

Convalescent plasma and AlloVirs coronavirus-specific T-cell therapies are not mutually exclusive, so they could even be used together.

More:
Equipping the Immune System to Fight Against COVID-19 - BioSpace

When our immune systems are fatigued by stress, inflammation, and poor nutrition, we feel tired and sluggish on a daily basis. Its hard to get out of bed even when we arent fighting a bug. Conversely, when our immune systems have the proper dietary support, they can fight off invading pathogens and help us recover more quickly.

What can you really do to boost your immunity? Nourish your body with healthy vitamins and foods.

Yes, thats all there is to it. When your body has the chemical compounds, it needs to synthesize white blood cells, repair cellular damage, and bounce back, your immune system is in peak form.

Below, well share our ten favorite foods and vitamins for improving immunity.

Fragrant orange turmeric is a staple of many healthy world cuisines.

Turmeric is powerfully anti-inflammatory thanks to the compound curcumin. What does that mean?

When your body responds to illness or stress by creating inflammation, your stress hormone levels rise, and your immune system goes on high alert. Soothing turmeric can help with chronic inflammation caused by insomnia, poor diet, and other factors.

Its also a great addition to curries, stews, and even grains.

When you lack Vitamin C, you get scurvy. What happens next? Your gums bleed, and your wounds dont heal. Its unpleasant, to say the least.

Vitamin C is crucial for cell repair and tissue healing. It can help with everything from post-exercise fatigue to the common cold.

How can you get it?

Garlic is a common folkloric cure for colds. Highly antibacterial and antifungal, its not just a great seasoning, but also a potent aid to your immune system. Try using the following in cooking:

Alternately, you can dip garlic cloves in honey and eat them raw. It may give you garlic breath, but we think its worth it.

Vitamin B6 helps your body synthesize red blood cells and neurotransmitters. Its most often found in:

You can also take it in a supplement.

Medicinal mushrooms are perhaps the next frontier of health. Long used in Traditional Chinese Medicine to promote longevity, shiitakes may also help your immune system to function well. These mushrooms are available at many grocery stores, or you can grow your own.

Bright, spicy ginger is a great addition to recipes from curry to ceviche. Better yet, its anti-inflammatory and antioxidant.

Ginger is also a traditional remedy for:

Pearl powder may not seem like a foodwe usually think of eating oysters, not their pearls! Indeed, pretty, translucent pearl powder is often found in skin care because of its nourishing properties.

However, pearl powder is full of:

These qualities make it the latest entrant to the hall of superfood fame.

Youve probably applied topical Vitamin E to cuts and scrapes. You also need plenty in your diet to support healthy immunity. Its vital for preventing the healthy flow of blood throughout the body, and your immune systems white blood cells need fast passage via the bloodstream to the site of any infection.

Find Vitamin E in:

Rich in antioxidants, elderberry syrup is a popular supplement for promoting immunity and heart health. In fact, its one of the most commonly used medicinal plants in the world!

You can also take it in a capsule, or find it in teas, gummies, and even lollipops.

While less exotic than some of the entrants on this list, green, leafy spinach is packed with beneficial nutrients:

Dont like to eat your greens? Throw it in the blender with some fruit and pretend its not there!

If you need more motivation to incorporate these healthy foods into your cooking repertoire, consider putting together a meal for friends and family. After all, healthy relationships actually help boost your immunity and overall health, too.

When it comes to supplements, make sure to use them daily to experience improved results over time.

Hopefully, your new routine helps you feel stronger and more ready for whatever comes your way.

See the article here:
10 Foods and Vitamins That Can Help Boost Your Immune System - South Florida Caribbean News

Cold and flu season always has us restocking our vitamin C supplies, but this year, as the pandemic continues and with the threat of a coronavirus-and-flu "twindemic" on the horizon, immune system health has become particularly important. (Quick PSA to get your flu shot.)

If you're looking into vitamins, minerals, and supplements to boost your immune system, go for it - but remember to do your research first. "For these kinds of questions, the gold standard of truth is the randomized controlled trial," said John Mafi, MD, MDH, an assistant professor of medicine in the Division of General Internal Medicine and Health Services Research at the David Geffen School of Medicine at UCLA. "While it's complicated to directly measure immune system strength, a good marker for it is how often or how long you get colds and flu viruses."

Ahead, we've rounded up a few of the vitamins and supplements that have proven benefits to your immune system so you can stock up as cold weather approaches.

-Additional reporting by Maggie Ryan

Link:
4 Essential Vitamins and Minerals to Boost Your Immune System This Year - MSN Money

Following the news this week of what appears to have been the first confirmed case of a Covid-19 reinfection, other researchers have been coming forward with their own reports. One in Belgium, another in the Netherlands. And now, one in Nevada.

What caught experts attention about the case of the 25-year-old Reno man was not that he appears to have contracted SARS-CoV-2 (the name of the virus that causes Covid-19) a second time. Rather, its that his second bout was more serious than his first.

Immunologists had expected that if the immune response generated after an initial infection could not prevent a second case, then it should at least stave off more severe illness. Thats what occurred with the first known reinfection case, in a 33-year-old Hong Kong man.

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Still, despite what happened to the man in Nevada, researchers are stressing this is not a sky-is-falling situation or one that should result in firm conclusions. They always presumed people would become vulnerable to Covid-19 again some time after recovering from an initial case, based on how our immune systems respond to other respiratory viruses, including other coronaviruses. Its possible that these early cases of reinfection are outliers and have features that wont apply to the tens of millions of other people who have already shaken off Covid-19.

There are millions and millions of cases, said Michael Mina, an epidemiologist at Harvards T.H. Chan School of Public Health. The real question that should get the most focus, Mina said, is, What happens to most people?

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But with more reinfection reports likely to make it into the scientific literature soon, and from there into the mainstream press, here are some things to look for in assessing them.

Whats the deal with the Nevada case?

The Reno resident in question first tested positive for SARS-CoV-2 in April after coming down with a sore throat, cough, and headache, as well as nausea and diarrhea. He got better over time and later tested negative twice.

But then, some 48 days later, the man started experiencing headaches, cough, and other symptoms again. Eventually, he became so sick that he had to be hospitalized and was found to have pneumonia.

Researchers sequenced virus samples from both of his infections and found they were different, providing evidence that this was a new infection distinct from the first.

What happens when we get Covid-19 in the first case?

Researchers are finding that, generally, people who get Covid-19 develop a healthy immune response replete with both antibodies (molecules that can block pathogens from infecting cells) and T cells (which help wipe out the virus). This is what happens after other viral infections.

In addition to fending off the virus the first time, that immune response also creates memories of the virus, should it try to invade a second time. Its thought, then, that people who recover from Covid-19 will typically be protected from another case for some amount of time. With other coronaviruses, protection is thought to last for perhaps a little less than a year to about three years.

But researchers cant tell how long immunity will last with a new pathogen (like SARS-CoV-2) until people start getting reinfected. They also dont know exactly what mechanisms provide protection against Covid-19, nor do they know what levels of antibodies or T cells are required to signal that someone is protected through a blood test. (These are called the correlates of protection.)

Why do experts expect second cases to be milder?

With other viruses, protective immunity doesnt just vanish one day. Instead, it wanes over time. Researchers have then hypothesized that with SARS-CoV-2, perhaps our immune systems might not always be able to prevent it from getting a toehold in our cells to halt infection entirely but that it could still put up enough of a fight to guard us from getting really sick. Again, this is what happens with other respiratory pathogens.

And its why some researchers actually looked at the Hong Kong case with relief. The man had mild to moderate Covid-19 symptoms during the first case, but was asymptomatic the second time. It was a demonstration, experts said, of what you would want your immune system to do. (The case was only detected because the mans sample was taken at the airport when he arrived back in Hong Kong after traveling in Europe.)

The fact that somebody may get reinfected is not surprising, Malik Peiris, a virologist at the University of Hong Kong, told STAT earlier this week about the first reinfection. But the reinfection didnt cause disease, so thats the first point.

The Nevada case, then, provides a counterexample to that.

What kind of immune response did the person who was reinfected generate initially?

Earlier, we described the robust immune response that most people who have Covid-19 seem to mount. But that was a generalization. Infections and the immune responses they induce in different people are heterogeneous, said Sarah Cobey, an epidemiologist and evolutionary biologist at the University of Chicago.

Older people often generate weaker immune responses than younger people. Some studies have also indicated that milder cases of Covid-19 induce tamer immune responses that might not provide as lasting or as thorough of a defense as stronger immune responses. The man in Hong Kong, for example, did not generate antibodies to the virus after his first infection, at least to the level that could be detected by blood tests. Perhaps that explains why he contracted the virus again just about 4 1/2 months after recovering from his initial infection.

In the Nevada case, researchers did not test what kind of immune response the man generated after the first case.

Infection is not some binary event, Cobey said. And with reinfection, theres going to be some viral replication, but the question is how much is the immune system getting engaged?

What might be broadly meaningful is when people who mounted robust immune responses start getting reinfected, and how severe their second cases are.

Are people who have Covid-19 a second time infectious?

As discussed, immune memory can prevent reinfection. If it cant, it might stave off serious illness. But theres a third aspect of this, too.

The most important question for reinfection, with the most serious implications for controlling the pandemic, is whether reinfected people can transmit the virus to others, Columbia University virologist Angela Rasmussen wrote in Slate this week.

Unfortunately, neither the Hong Kong nor the Reno studies looked at this question. But if most people who get reinfected dont spread the virus, thats obviously good news.

What happens when people broadly become susceptible again?

Whether its six months after the first infection or nine months or a year or longer, at some point, protection for most people who recover from Covid-19 is expected to wane. And without the arrival of a vaccine and broad uptake of it, that could change the dynamics of local outbreaks.

In some communities, its thought that more than 20% of residents have experienced an initial Covid-19 case, and are thus theoretically protected from another case for some time. That is still below the point of herd immunity when enough people are immune that transmission doesnt occur but still, the fewer vulnerable people there are, the less likely spread is to occur.

On the flip side though, if more people become susceptible to the virus again, that could increase the risk of transmission. Modelers are starting to factor that possibility into their forecasts.

A crucial question for which there is not an answer yet is whether what happened to the man in Reno, where the second case was more severe than the first, remains a rare occurrence, as researchers expect and hope. As the Nevada researchers wrote, the generalizability of this finding is unknown.

Read more:
Several have been reinfected with Covid-19. Here's what that means - STAT

Most people are aware that testing for antibodies in a persons blood can show if someone has had a specific disease, such as COVID-19. Those antibodies provide protection from getting the disease again.

But in a paper published in the New England Journal of Medicine, researchers found that antibody levels decline in individuals who have recovered from COVID-19, dropping by half every 36 days. Does that mean people who have recovered from COVID-19 have lost their immunity?

I am a geneticist interested in innate immune response the part of the immune system that we have at birth and how the innate immune cells educate antibody-producing cells about a pathogen and how to identify and destroy it. As Ill explain, antibodies are important for immunity, but they arent the only factor that counts.

The immune system is made up of two parts: innate immunity and adaptive or acquired immunity.

The innate immune system, which includes white blood cells called dendritic cells, monocytes and neutrophils, is present at birth and responds instantly to invaders. This group of white blood cells bombard pathogens with destructive chemicals and swallow and destroy viruses and bacteria. The innate immune system provides an instantaneous reaction to a pathogen. The problem is that its a blunt instrument it responds the same way to all perceived threats.

The adaptive immune system, which is made up of B cells and T cells, must learn about a pathogen and its characteristics from the innate immune cells. This system takes longer to kick in, but the up side is that it is very specific and in many cases lasts a lifetime.

The history of pathogen exposure is carried in so-called memory T cells and memory B cells. When an infection is defeated and gone, these cells reside in the peripheral tissues of the body such as lymph nodes or spleen and serve as a memory of the disease-causing virus. This immunological memory is responsible for the host defense and kicks into action in case of the second wave or attack of the pathogen.

It is normal for antibody levels to decline after a person has recovered from a disease. But the New England Journal of Medicine paper raised concerns because it suggests that we are losing our immunological memory which is as bad as losing a real memory.

B cells and antibodies are only part of the immune response. T cells help B cells produce antibodies which are proteins that can bind to a specific pathogen and destroy it.

The way this happens is that first the B cells swallow the virus and start producing antibodies.

T cells cannot swallow the virus. But a type of white blood cell called an antigen-presenting cell can. After it does, it shows different parts of the virus to the T cells. The T cells then learn about the virus which they can now seek and destroy.

T cells also stick to the B cells and send them the activation signals that help B cells ramp up antibody production.

It suggests that when there are fewer antibodies in the blood, there is a greater chance that a number of individual virus particles, called virions, will survive and escape destruction. Therefore, the remaining virions will continue to proliferate and cause disease.

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Herd immunity refers to a population and occurs when a sufficiently high number of people within a community are immune to the virus and incapable of transmitting it. That provides protection for those who are still vulnerable. For example, if 60% of people are protected against COVID because they have survived the infection and carry antibodies it might protect (via less frequent interactions) the remaining 40% from getting sick.

But the results in the New England Journal of Medicine suggest that people with lower levels of antibody may still have the virus and may not have symptoms of the disease.

That means that if these people with low antibody levels hang around healthy, uninfected people, they present a danger to them because they can transmit the virus.

In general, the answer is no. If the virus attempts to cause a second infection, the memory B and T cells are able to recognize it, multiply million of times and defend the body against the virus, preventing it from triggering another full-blown infection.

The protection provided by memory T and B cells is the reason that vaccine-based protection works.

However, there are exceptions. A lifelong vaccine against the flu does not work because flus genetic code changes rapidly, altering the appearance of the flu, and therefore requires a new vaccine every season.

But with SARS-CoV-2, the problem as I see it, seems to be that those memory T cells and B cells seem to be wiped out.

Antibodies are proteins and last for only between three and four weeks in the blood circulation. To keep antibody levels high, B cells need to replenish them with a fresh supply. But in COVID-19, the declining antibody levels suggest that the cells that produce these antibodies are not present in sufficient numbers, which would explain the drop in antibody levels. Studies of how long immunity from COVID-19 last may shed more light, but for now we do not know the reason why.

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Declining antibodies and immunity to COVID-19 why the worry? - The Conversation US

Something that gave me an even greater incentive to write my book, The 21 Day Immunity Plan, was the premature deaths of two family members who suffered and died because of a compromised immune system.

My older brother, Amit, died of a virus that affected his heart at the age of 13. Born with Downs syndrome, his compromised immune system was genetic and there was little that could have been done to prevent his death from crashing heart failure when he caught a tummy bug that most people would have been able to fight off.

The second was my mother, who over the four-week period of her final admission to hospital endured indescribable pain from an infection that affected her spine. Her compromised immune system was almost entirely rooted in lifestyle choices. Because the NHS was already overstretched, a heart attack was missed, treatment was delayed and she gasped for breath as fluid engulfed her lungs. Eventually she slipped into a coma as the infection spread through her body, and she passed away aged only 68.

Beyond my observations as a medical scientist and my duties as a clinical doctor to share knowledge on the link between metabolic health and immunity, I wrote my book from the perspective and motivation of someone who has had to deal with all the emotion and sadness of seeing a close family member die well before their time and in the most horrible of circumstances. No one needs to suffer like she did and no family member should have to witness it.

What Covid-19 has also done is expose areas in our health systems and personal well-being that have long been neglected, and which in themselves have made us more vulnerable to such a particularly pernicious virus. But in spite of the tragedy, the disturbing statistics and heartbreaking stories that have collectively gripped the world, we can draw from the lessons the virus has taught us and look to a brighter future.

The 21-day immunity plan is one that involves nutritious food, helps to regulate and reduce inflammation, combats insulin resistance and improves overall metabolic health. It should be enjoyable and be in keeping with all cultures and personal preferences.

It will help you to:

Over the course of the three weeks, you will follow an eating plan, you will be required to move your body daily, carry out breathing exercises, monitor and improve your sleep habits and be seeking to reduce your stress and improve your mental well-being by making a concerted effort to nurture and celebrate time with friends and family.

Please note that if you suffer from type 2 diabetes, high blood pressure or heart disease and more specifically are taking medications, you must consult your doctor before starting the 21-day plan, as medication is likely to need adjusting/reducing and may potentially need to be stopped altogether.

We know that prolonged sitting and being more sedentary in general increases the risk of heartdisease, high bloodpressure and type 2 diabetes.

Regular cardiovascular exercise has the strongest evidence base when it comes to reducing the risk of many diseases. It has even been shown to significantly reduce insulin resistance within three months for those who start off with a sedentary lifestyle, even without weight loss.

Throughout the three weeks of this plan, I want you to go for a brisk walk for at least 30 minutes on five days each week. Subjectively, this is where you feel a bit out of breath to the point youre able to have a conversation but youll find it difficult to sing.

If you want to be very precise, then measuring your heart rateprovides a more objective measure of activity intensity.

You want to aim to get your heart rate within a range of 50 to 70 per cent ofyour maximum, which isrelated to your age. Thereason for this heart-rate range is based on numerous studies which reveal beneficial physiological changes in thebody startto occur once you exerciseat this level, including reduced insulinresistance.

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The 21-day plan to support your immune system and help fight off infections - Telegraph.co.uk

By: New York Times | Published: August 28, 2020 9:31:47 amThe two studies, which involved the same group of elite runners, swimmers, wrestlers, cyclists and other athletes, suggest that intense training amplifies our vaccine response. (PTI/File)

Written by Gretchen Reynolds

Two new studies of elite athletes found that working out amplifies the immune response to a flu shot.

If you are an athlete, you may gain greater immunity from a flu shot than people who are less active, according to two complementary and timely new studies of exercise and vaccinations. The two studies, which involved the same group of elite runners, swimmers, wrestlers, cyclists and other athletes, suggest that intense training amplifies our vaccine response, a finding with particular relevance now, as the flu season looms and scientists work to develop a COVID-19 vaccine.

Having an immune system primed to clobber infections and respond robustly to vaccinations is obviously desirable now, during the ongoing pandemic. And in general, exercise aids immunity, most science shows. People who work out often and moderately tend to catch fewer colds and other viruses than sedentary people. More immediately, if you exercise your arm in the hours before a flu shot, you likely willdevelop a stronger antibody responsethan if you rest that arm, a few small studies indicate.

But there have also been suggestions that under certain circumstances, exercise may dampen the immune response. Some epidemiological research and personal stories from athletes hint that intense, exhausting exercise might be detrimental to immunity in the short term.Marathon racers, for example, report catching colds at disproportionately high rates soon after a race, although some physiologists suspect thesepost-race respiratory problems are inflammatory, not infectious.

The upshot, though, is that many questions have remained unanswered about whether and how strenuous workouts affect immunity and our bodies ability to respond favorably to a vaccination, such as the seasonal flu shot.

So, for the new studies, scientists from Saarland University in Germany and other institutions decided to convince a large group of competitive athletes to get vaccinated, an effort more difficult than most of us might expect. In surveys, elite athletes tend to report relatively low rates of vaccination for the flu and other conditions, since many worry the shot will cause side effects that affect their training.

But the researchers managed to recruit 45 fit, young, elite athletes, male and female. Their sports ranged from endurance events, like the marathon, to power sports, including wrestling and hammer throw, to team sports, such as basketball and badminton. All of the volunteers were in the middle of their competitive seasons during the studies.

For the first of the two experiments involving these athletes, which waspublished in January in Brain, Behavior, and Immunity, the researchers hoped to establish whether being an athlete and having an athletes outsized fitness would goose or impede the young peoples immune reaction to a flu shot. So, the scientists also recruited an additional 25 young people who were healthy but not athletes to serve as a control group. They drew blood from everyone.

Afterward, all of the young people received a flu shot and kept notes about any side effects they felt, such as a sore arm. The groups returned to the lab for follow-up blood draws a week, two weeks and six months after the vaccination. Then the researchers checked their blood for anti-influenza immune cells and antibodies.

They found significantly more of those cells in the athletes blood, especially in the week after the shot, when everyones cellular reactions peaked. The athletes showed a more pronounced immune response, with presumably better protection against flu infection than the other young people, says Martina Sester, an immunologist at Saarland University and study co-author.

The researchers speculate that the athletes immune systems had been strengthened and fine-tuned by the daily physical demands and damages of training, allowing them to respond so effectively to the vaccine.

But those results, while notable, did not look at the acute effects of exercise and whether a single, intense workout might alter the bodys reactions to a vaccine, for better or worse. So, for the second of the new studies, which waspublished in July in Medicine & Science in Sports & Exercise, the scientists returned to the same data, but focused now only on the immune reactions of the athletes.

They compared the numbers of immune cells and antibodies in those athletes who happened to have gotten their flu shot within two hours of their most recent training session against those of athletes whose shot had come a day after their last workout. If intense training blunted immune reactions, then the first group of athletes would be expected to show fewer new immune cells than those who had gotten their shot after a longer rest.

But the researchers found no differences. Whether the athletes inoculations came almost immediately after training or a day later, their immune reactions were the same. A strenuous workout beforehand had not lowered or boosted the response.

Together, the two studies tell us that being in shape is likely to increase our protection from a vaccination, no matter how intensely or when we work out before the shot, Sester says.

Of course, these studies focused on elite, competitive athletes, which most of us are not. But Sester believes even more-casual recreational athletes are likely to mount better flu-vaccine responses than sedentary people. Likewise, she and her colleagues expect high fitness should improve immune responses to other vaccines, including, potentially, a COVID-19 shot.

The basic principles of vaccine response are probably the same, she says. Future studies will have to confirm that possibility, though, if and when a vaccine becomes available.

The Indian Express is now on Telegram. Click here to join our channel (@indianexpress) and stay updated with the latest headlines

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Exercise may boost your vaccine response - The Indian Express

Amid this week's news that a man in Hong Kong was reinfected with the novel coronavirus, STAT News Hellen Branswell asked health experts to predict how different types of immunity to the novel coronavirus, or a lack thereof, could dictate what a future with the virus would look like.

Researchers have been working to understand whether exposure to the novel coronavirus could protect people from future infection. Questions regarding immunity to the coronavirus haven't yet been answered definitively, but researchers have pointed to some preliminary evidence suggesting that people infected with the virus develop antibodies and other immune responses that could protect them against reinfection for at least several months to potentially a few years.

However, some health care providers have reported cases in which patients appeared to become reinfected with the virus. And on Monday, researchers in Hong Kong confirmed the first documented case of novel coronavirus reinfection. According to the researchers, a 33-year-old man who was first diagnosed with a novel coronavirus in March, and who had recovered from that infection, was later infected with a different strain of the virus that had been spreading throughout Europe in July and August.

That case has spurred even more questions about the type of immunity people may develop to the novel coronavirus, Branswell reports. Recently, she asked health experts to predict how different types of immunity to the virus, or a lack thereof, could dictate what a future with the virus would look like, and Vineet Menachery, a coronavirus researcher at the University of Texas Medical Branch, came up with four different scenarios that are quite "hopeful," Branswell writes. However, she cautions that the scenarios described are merely "educated guesses, based on what's known about the way the immune system works in general, and how it responds to other coronaviruses."

Sterilizing immunity

The best-case scenario, Branswell writes, would be so-called "sterilizing immunity," which can fight off a virus "before infection can take hold."

According to Branswell, this type of immunity usually occurs when the body incurs a pathogen that induces strong and durable immune responses during initial infection, such as measles. But unfortunately for the current crisis, respiratory viruses that infect the mucus membranes in the nose and throatsuch as the novel coronavirusdon't usually result in sterilizing immunity.

"Sterilizing [immunity] in my view is out of the question, as with any respiratory virus," said Marion Koopmans, head of virology at Erasmus Medical Center in the Netherlands.

Stanley Perlman, a researcher at the University of Iowa, seemingly agreed, noting it was "not so likely" the novel coronavirus will induce sterilizing immunity.

The low likelihood that infection from the coronavirus can induce sterilizing immunity has raised concerns that a vaccine against the virus wouldn't be able to generate sterilizing immunity, either, Branswell writes. It's also sparked concerns that a vaccine wouldn't prevent the virus' spreadeven though it might reduce the severity of Covid-19, the disease caused by the virus.

"[W]e'd all like immunity that protects the individualprotects from infection and protects from transmission," said Malik Peiris, a coronavirus expert at Hong Kong University, but "[w]e may not achieve that, because protecting from infection of the upper respiratory tract and then transmission is quite a challenge."

Functional immunity

However, one type of immune response that may be "within reach," according to Branswell, is "functional immunity," which occurs when a body recognizes a pathogen, either due to a previous infection or vaccination. While people who develop this type of immunity could become reinfected with the pathogen at a later date, they would experience a milder, shorter infection.immunity, immunity, people who

"It may be possible to become infected again, without any change in the virus," said Christian Drosten, director of the Institute of Virology at Berlins Charit University Hospital. But "[t]he resulting infection will be mild or asymptomatic, with significantly lower levels of virus replication and onward transmission."

So ultimately, even though there would still be cases of coronavirus infection and Covid-19, the disease "won't have the impact it has now" under this immunity scenario, Peiris said. "It becomes manageable."

And, according to the experts, the immune responses we've seen so far to the novel coronavirus are in line with what they'd expect to see under this scenarioincluding in the recent Hong Kong case. While the man in that case experienced symptoms of Covid-19 during his first infection, he reportedly didn't experience Covid-19 symptoms during the second infection.

For his part, Menachery said he thinks it's likely that most people will develop functional immunity to the novel coronavirus.

"The idea there is that, yes, your antibodies might wane, but your memory responses aren't absent," he said. "I'm a believer that if you've gotten Covid-19, then your likelihood of dying from a second Covid-19 case is very low, if you maintain immunity."

And if people who are reinfected experience a lesser infection, they might also generate lower levels of the virus, meaning they could be less likely to pass it on, Branswell reports. "It may become a rare infection, although that is difficult to foresee given the size of the global population," Koopmans said.

In addition, children, who appear less likely to develop severe cases of Covid-19 than adults, might never experience a severe case of the disease after developing functional immunity over their lifetimes. "I think that's kind of how, in the long run, it would play out without the intervention of vaccines," Krammer said. "I think with vaccines, we just basically speed up that process."

However, experts warned of one big question regarding this type of immunity: Whether and to what extent people whose first infections did not result in symptoms of Covid-19, or who had very mild cases, would develop this longer-lasting immune response. Perlman was cautiously hopeful, saying he would hypothesize that such individuals would have sufficient protection against severe cases of the disease.

Waning immunity

The third scenario involves a variant of functional immunity called "waning immunity," Branswell writes, in which people who have been infected with or vaccinated against the novel coronavirus could experience a decreased level of protection over time. According to Branswell, this type of immune response is seen with four coronaviruses that cause common colds and can reinfect people "after a relatively short period of time."

For example, one Dutch study, which has not yet been peer reviewed, measured antibody levels for those four coronaviruses in 10 people for decades and "saw frequent reinfections at 12 months postinfection and substantial reduction in antibody levels as soon as six months postinfection," the researchers wrote.

Lia van der Hoek from Amsterdam University Medical Center, a senior author of the study, said she thinks waning immunity is the most likely immune response for people infected with the novel coronavirus.

But, she added, "It is completely unknown what the symptoms will be when reinfection occurs. This could be less, or worse, or equal. We scientists cannot make a prediction on that."

For his part, Menachery said he believes that, even if immunity faded over time, the reinfections would still be less severe. "You will never get as sick as you were the first time," Menachery said.

Lost immunity

A more dire scenario, according to Branswell, would be so-called "lost immunity," in which people who have previously been infected with the coronavirus lose immunity against the virus within a certain timeframeafter which point, any reinfection could be as severe as the first.

However, Branswell writes that "[n]one of the experts felt this was a possibility."

Menachery said people who "generate a response to clear the virus" will likely "maintain that immunity long term." However, he added that, for "people with mild or asymptomatic infection, it may not be lost immunity, but rather no immunity generated."

And overall, Branswell writes, if lost immunity is unlikely, then we will probably see the threat of Covid-19 decrease over time. "Our immune systems will know how to deal with" the novel coronavirus, she writes. "It could become the fifth human coronavirus to cause common colds."

But Dan Barouch, director of the Center for Virology and Vaccine Research at Boston's Beth Israel Deaconess Medical Center, warned that it might take a long time to reach such a point. According to Barouch, the majority of the world's population has yet to be exposed to the novel coronavirusand vaccinating everyone in the world could take years.

Further, Barouch added that it's unlikely only one of these immunity scenarios would occur. He explained that immunity often depends on a person's immune system, as well as the nature of their exposure to a pathogen. "The short answer is we don't know. So, anyone who gives you a scenario is providing a hypothesis," he said (Branswell, STAT News, 8/25).

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What does 'immunity' to Covid-19 really mean? Here are 4 possibilities. - The Daily Briefing

The severity of COVID-19 can vary hugely. In some it causes no symptoms at all and in others its life threatening, with some people particularly vulnerable to its very severe impacts.

The virus disproportionately affects men and people who are older and who have conditions such as diabetes and obesity. In the UK and other western countries, ethnic minorities have also been disproportionately affected.

While many factors contribute to how severely people are affected, including access to healthcare, occupational exposure and environmental risks such as pollution, its becoming clear that for some of these at-risk groups, its the response of their immune system inflammation that explains why they get so sick.

Specifically, were seeing that the risks associated with diabetes, obesity, age and sex are all related to the immune system functioning irregularly when confronted by the virus.

Inflammation can go too far

A common feature for many patients that get severe COVID is serious lung damage caused by an overly vigorous immune response. This is characterised by the creation of lots of inflammatory products called cytokines the so-called cytokine storm.

Cytokines can be really powerful tools in the immune response: they can stop viruses reproducing, for example. However, some cytokine actions such as helping bring in other immune cells to fight an infection or enhancing the ability of these recruited cells to get across blood vessels can cause real damage if they are not controlled. This is exactly what happens in a cytokine storm.

Many white blood cells create cytokines, but specialised cells called monocytes and macrophages seem to be some of the biggest culprits in generating cytokine storms. When properly controlled, these cells are a force for good that can detect and destroy threats, clear and repair damaged tissue, and bring in other immune cells to help.

However, in severe COVID the way monocytes and macrophages work misfires. And this is particularly true in patients with diabetes and obesity.

Diabetes, if not controlled well, can result in high levels of glucose in the body. A recent study showed that, in COVID, macrophages and monocytes respond to high levels of glucose with worrying consequences.

The virus that causes COVID, SARS-CoV-2, needs a target to latch onto in order to invade our cells. Its choice is a protein on the cell surface called ACE2. Glucose increases the levels of ACE2 present on macrophages and monocytes, helping the virus infect the very cells that should be helping to kill it.

Cytokines, small proteins released by a number of immune cells, play a key role in directing the immune response.

Image: scientificanimations.com

Once the virus is safely inside these cells, it causes them to start making lots of inflammatory cytokines effectively kick-starting the cytokine storm. And the higher the levels of glucose, the more successful the virus is at replicating inside the cells essentially the glucose fuels the virus.

But the virus isnt done yet. It also causes the virally infected immune cells to make products that are very damaging to the lung, such as reactive oxygen species. And on top of this, the virus reduces the ability of other immune cells lymphocytes to kill it.

Obesity also causes high levels of glucose in the body and, similar to diabetes, affects macrophage and monocyte activation. Research has shown that macrophages from obese individuals are an ideal place for SARS-CoV-2 to thrive.

Other risks tied to inflammation

The same sort of inflammatory profile that diabetes and obesity cause is also seen in some older people (those over 60 years). This is due to a phenomenon known as inflammageing.

Inflammageing is characterised by having high levels of pro-inflammatory cytokines. Its influenced by a number of factors, including genetics, the microbiome (the bacteria, viruses and other microbes that live inside and on you) and obesity.

Many older people also have fewer lymphocytes the very cells that can specifically target and destroy viruses.

This all means that for some older people, their immune system is not only poorly equipped to fight off an infection, but it is also more likely to lead to a damaging immune response. Having fewer lymphocytes also means vaccines may not work as well, which is crucial to consider when planning a future COVID vaccine campaign.

Irregular inflammatory responses are emerging as a common theme across the different risk factors for severe COVID.

Image: EPA-EFE

Another puzzle that has been worrying researchers is why men seem so much more vulnerable to COVID. One reason is that cells in men seem to be more readily infected by SARS-CoV-2 than women. The ACE2 receptor that the virus uses to latch onto and infect cells is expressed much more highly in men than women. Men also have higher levels of an enzyme called TMPRSS2 that promotes the ability of the virus to enter the cells.

Immunology is also offering some clues on the sex difference. Its long been known that men and women differ in their immune responses, and this is true in COVID.

A recent pre-print (research that has not yet been reviewed) has tracked and compared the immune response to SARS-CoV-2 in men and women over time. It found that men were more likely to develop atypical monocytes that were profoundly pro-inflammatory and capable of making cytokines typical of a cytokine storm. Women also tended to have a more robust T cell response, which is needed for effective virus killing. However, increased age and having a higher body mass index reversed the protective immune effect in women.

Studies like these highlight how different people are. The more we understand about these differences and vulnerabilities, the more we can consider how best to treat each patient. Data like these also highlight the need to consider variation in immune function and include people of varied demographics in drug and vaccine trials.

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How does the immune response affect inflammation in COVID-19 patients? - World Economic Forum

You dont really want to "boost" your immune system.

Q: I always seem to get sick when I start a job. Makes sense new people, new germs. I started a job in February, then we all had to work from home. I worry that being isolated for weeks puts me back at square one. What can I ado to boost my immunity in preparation for going back to the office?

A: We're always happy to have this particular discussion, because the strategies and habits involved in addressing immune health also tend to lead to improved health overall. The immune system plays an important role in protecting us from all sorts of potential pathogens, and you're not alone in wondering how to give it an edge.

First, let's clarify the goal. We hear a lot about "boosting" the immune system, but that's actually misleading. You don't want an amped-up immune system. That would mean that it's hyper-alert and reacts and overreacts to every perceived threat. Rather, the goal is an immune system that's healthy and balanced and responds in proportion to the job at hand.

One of the most important steps you can take to keep your immune system happy and healthy involve lifestyle. That is, get an adequate amount of high-quality sleep, take part in daily exercise, don't smoke, limit alcohol use and eat a healthful diet. When you're chronically tired, depressed or anxious, overweight, eat poorly, smoke, drink too much and don't get enough exercise, you're creating internal stressors that can interfere with optimal immune system response.

Diet plays an important role in immune system health. Emerging research continues to link the health and diversity of the gut microbiome with the health and efficacy of the immune system. We urge our patients to get the necessary vitamins and minerals through food, which we believe the body utilizes more efficiently than supplements. Plenty of fresh vegetables, leafy greens and fruit are crucial to getting a range of vitamins and minerals and to keeping the billions of microorganisms that make up our gut microbiomes well-fed. So are nuts, seeds, beans and legumes. Cultured and fermented foods, such as pickles, sauerkraut, yogurt, kombucha, kefir and miso help with diversity.

We know it's a challenge, but steering clear of added sugar, sugary soft drinks and highly processed foods is also important to both gut and immune health. Recent studies have shown that regular exercise improves gut health. Sleep is also critical to health and well-being. We've had a lot of readers asking for help in this area, and we will revisit the topic in a column in the next few weeks.

We understand that, compared with the vitamins and supplements and products that promise instant immune system magic, this advice sounds pretty dull. But our bodies are intricate and interconnected mechanisms. Everything from circadian rhythms, which are affected by sleep, to the gut microbiome, which is affected by diet and exercise, to mood, which responds to all three, play a role in immune health. Focusing on a whole-body approach, with gradual but consistent changes, goes a long way toward building an immune system that's balanced and ready to work for you.

Send your questions to askthedoctors@mednet.ucla.edu, or write: Ask the Doctors, c/o UCLA Health Sciences Media Relations, 10880 Wilshire Blvd., Suite 1450, Los Angeles, CA, 90024.

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Boosting the immune system could offer a potential treatment strategy for COVID-19, according to a new study.

As the COVID-19 pandemic continues to claim lives around the world, much research has focused on the immune systems role in patients who become seriously ill.

A popular theory has it that the immune system gets so revved up fighting the virus that, after several days, it produces a so-called cytokine storm that results in potentially fatal organ damage, particularly to the lungs.

Some drugs tamp down the immune response, while others enhance it. Everybody seems to be throwing the kitchen sink at the illness.

But the new findings point to another theory and suggest that patients become ill because their immune systems cant do enough to protect them from the virus, landing them in intensive care units.

Researchers detailed the new strategy to boost the immune system in two papers, in JAMA Network Open and in the journal JCI Insight.

People around the world have been treating patients seriously ill with COVID-19 using drugs that do very different things, says senior investigator Richard S. Hotchkiss, professor of anesthesiology, of medicine, and of surgery at Washington University in St. Louis.

Some drugs tamp down the immune response, while others enhance it. Everybody seems to be throwing the kitchen sink at the illness. It may be true that some people die from a hyperinflammatory response, but it appears more likely to us that if you block the immune system too much, youre not going to be able to control the virus.

We think if we can make our immune systems stronger, well be better able to fight off this coronavirus

The researchers have been investigating a similar approach in treating sepsis, a potentially fatal condition that also involves patients who simultaneously seem to have overactive and weakened immune systems.

Hotchkiss points to autopsy studies performed by other groups showing large amounts of coronavirus present in the organs of people who died from COVID-19, suggesting that their immune systems were not working well enough to fight the virus.

His colleague, Kenneth E. Remy, first author of the JCI Insight paper, compares efforts to inhibit the immune system to fixing a flat tire by letting more air out.

But when we actually looked closely at these patients, we found that their tires, so to speak, were underinflated or immune-suppressed, says Remy, assistant professor of pediatrics, of medicine, and of anesthesiology.

To go and poke holes in them with anti-inflammatory drugs because you think they are hyperinflated or hyperinflamed will only make the suppression and the disease worse.

After gathering blood samples from 20 COVID-19 patients at Barnes-Jewish Hospital and Missouri Baptist Medical Center in St. Louis, the researchers employed a test to measure the activity of immune cells in the blood. They compared the blood of those patients to 26 hospitalized sepsis patients and 18 others who were very sick but had neither sepsis nor COVID-19.

They found that the COVID-19 patients often had far fewer circulating immune cells than is typical. Further, the present immune cells did not secrete normal levels of cytokinesthe molecules many have proposed as a cause of organ damage and death in COVID-19 patients.

Instead of trying to fight the infection by further interfering with the production of cytokines, they tried a strategy that has been successful in previous studies they have conducted in sepsis patients.

Hotchkiss and Remy collaborated with researchers in a small study conducted in seriously ill hospitalized COVID-19 patients in Belgium.

In that study, which the researchers reported on in the JAMA Network Open paper,researchers treated the COVID-19 patients with a substance called interleukin-7 (IL-7), a cytokine, required for the healthy development of immune cells.

In those patients, the researchers found that IL-7 helped restore balance to the immune system by increasing the number of immune cells and helping those cells make more cytokines to fight infection.

The research did not demonstrate, however, that treatment with IL-7 improved mortality in COVID-19 patients.

This was a compassionate trial and not a randomized, controlled trial of IL-7, Remy explains. We were attempting to learn whether we could get these immune cells working againand we couldas well as whether we could do it without causing harmful effects in these very sick patientsand there were none.

As this was an observational study involving a small number of patients who already were on ventilators, it wasnt really designed to evaluate IL-7s impact on mortality.

Studies focused on boosting immunity and improving outcomes among the sickest COVID-19 patients are just getting underway in Europe, and similar trials are starting in the US, including at Washington University.

Finding ways to boost the immune response should help not only in COVID-19 patients but when the next pandemic arises, Hotchkiss says.

We should have been geared up and more ready when this pathogen appeared, he says. But what Ken and I and our colleagues are working on now is finding ways to boost the immune system that may help people during future pandemics. We think if we can make our immune systems stronger, well be better able to fight off this coronavirus, as well as other viral and bacterial pathogens that may be unleashed in the future.

Source: Washington University in St. Louis

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Can boosting the immune system treat COVID-19? - Futurity: Research News

Any new infectious disease poses unique challenges to people who are pregnant during an outbreak. The effects of Sars, Zika and influenza in pregnancy highlight the potential immediate and longer term detrimental health outcomes a virus can have for both mother and baby. These risks include premature delivery of the baby with Sars, birth defects with Zika and greater risk of severe influenza.

Should we be as worried about pregnancy and COVID-19? There are a number of things we need to think about. These fall into two broad areas related to the effects on the foetus and the effects on the pregnant person themselves.

In both cases we need to think about the immediate effects during the pregnancy as well as the longer term health effects for both parent and child. The early evidence we have shows that changes to the immune system during pregnancy could be somewhat protective against the disease.

Early data from pregnant women with COVID-19 indicates that the disease is linked to premature birth and changes to the placenta that might reflect altered blood flow. This suggests that virus-associated disruptions do occur between parent and foetus.

However, these studies were of women with severe cases of the disease. We know very little about the effect of mild disease or asymptomatic infection in pregnancy. Understanding this is critical, as studies have highlighted that asymptomatic and mildly infected pregnant women far outnumber those requiring hospitalisation for COVID-19.

This indicates that pregnant people are not more susceptible to severe COVID-19, which was one of the greatest concerns at the beginning of the pandemic and led to them being categorised as vulnerable.

The apparent protective effect of pregnancy against severe disease might simply reflect the different immune responses to severe COVID-19 seen in men and women, and the fact that more men than women die from the disease in general. However, we do not see the same response in pregnancy with other viruses, such as influenza, suggesting something else is at play with SARS-CoV-2.

So far, it seems that the foetus is very well protected from the passage of SARS-CoV-2 from mother to child (known as vertical transmission) and such passage, while possible, seems to be uncommon. This might be down to the natural features of the placenta, which produces molecules that stop the virus binding to placental cells. It could also be that the placental membranes limit infection by the virus.

Of course, it is very difficult to study the placenta prior to birth. Alternative measures, such as analysing cellular debris released from the placenta (known as extracellular vesicles) which can be found in a sample of the mothers blood, are really needed to find out what features of the placenta might protect the foetus from infection and what effects the virus has on the placenta.

Any antibodies that a mother infected with SARS-CoV-2 makes will pass to the foetus across the placenta (known as passive immunity). This provides short-term protection from many infectious agents for the last months of pregnancy and for some months after the baby is born. These antibodies will also continue to be provided in breast milk if the baby is breast fed.

Early studies from China have shown that antibodies that protect against COVID-19 are present in newborns of women who had such antibodies. This confirms that passive immunity, where a baby essentially inherits antibodies from a parent, occurs with SARS-CoV-2. We now need some larger studies to investigate whether anti-SARS-CoV-2 antibodies are present in human milk to better understand the role of these antibodies in neutralising the virus and protecting the baby.

Molecules other than antibodies can also pass from parent to foetus. Pregnant women with severe COVID-19 have many of the hallmarks of an inflammatory response that we see in other people with similar symptoms. This includes elevated levels of molecules such as interleukin-6 (IL-6), which indicates that the immune response has been activated.

There are a number of studies showing that maternal immune activation can have detrimental effects on the developing foetus. Such activation is associated with increased risk of respiratory, cardiovascular, neurodevelopmental and other disorders in the offspring. Whether SARS-CoV-2 will have such long-term effects on the health of these children remains to be seen.

In a previous article, we discussed how the immune system changes during pregnancy, and it might be that unique features of this and other dynamic adaptations that occur with pregnancy provide protection from severe COVID-19.

Other examples of possible protective mechanisms include differences in the receptor molecules used by SARS-CoV-2 to invade human cells. Angiotensin-converting enzyme 2 (ACE2) is the best known of these viral entry receptors but CD147, CD26 and others also have this role.

All of these receptors undergo changes during pregnancy, which might contribute to resilience. These receptors also occur as soluble forms that can be measured in blood and breast milk and might act as decoy receptors, stopping the virus from binding to cells.

Elaborating on why both the pregnant person and their child seem to be relatively resilient to severe forms of COVID-19 might help us understand other disease processes and identify ways to combat the disease.

Work from the UK Obstetric Surveillance System has shown that, as with the wider population, Asian and Black pregnant women are more likely to be admitted to hospital with SARS-CoV-2 infection. Therefore, we really need to consider the effects of ethnicity and other risk factors in our studies of COVID-19 in pregnancy.

This is especially important as these studies will support efforts towards the use of any vaccine in pregnancy.

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COVID-19 and pregnancy: what we know about what happens to your immune system - The Conversation UK

By: Express News Service | New Delhi | Updated: August 14, 2020 9:11:20 amA doctor attends to a Covid-19 patient in Argentina. (AP Photo: Natacha Pisarenko)

Why are some Covid-19 cases more severe than others? A new study has uncovered deviations and lapses in the immune system that appear to spell the difference between severe and mild cases of Covid-19.

The difference, the study suggests, may stem from how our evolutionarily ancient innate immune system responds to SARS-CoV-2, the novel coronavirus that cases Covid-19. The innate immune system rapidly senses pathogens, and immediately launches a somewhat indiscriminate attack on them. It also mobilises precisely targeted, but slower sharp-shooter cells from the adaptive immune system (which is different from the innate immune system).

These findings reveal how the immune system goes awry during coronavirus infections, leading to severe disease, and point to potential therapeutic targets, senior author Bali Pulendran of Stanford Medicine said in a statement. The study is published in Science.

The researchers analysed the immune response in 76 people with Covid-19 and in 69 health people. They found enhanced levels of molecules that promote inflammation in the blood of severely ill patients. Three of these molecules are known to be associated with lung inflammation in other diseases, but had not been shown previously in Covid-19 infections.

Source: Stanford Medicine News Center

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Explained: How the immune system goes awry in severe Covid-19 cases - The Indian Express

Alcohol abuse is a serious problem worldwide. In England alone, over 350,000 alcohol-related hospital admissions and over 5,000 alcohol-related deaths were reported in 2018. Long-term alcohol abuse can have many harmful effects on our body. But one of the organs most affected by alcohol is the brain. Even moderate consumption changes brain structure and leads to cognitive issues, such as declines in memory and problem-solving.

Alcohol use is habit forming and can eventually lead to alcoholism. And though there are many treatments available for alcoholism, research shows these interventions often fail with less than 20% of patients remaining alcohol free after intervention. Like every addiction, alcoholism is a disease and not a choice, so finding the root cause of it will make treatment easier.

Although genetics and the environment you live in are known to play a role in developing alcoholism, these factors dont tell us how dependence occurs.

However, past research has found hints that the brains immune system cells (known as microglia) may be involved in addiction, including to cocaine and tobacco). One study even found that alcohol exposure and withdrawal in rats increased microglia numbers in the brain, before any other signs of alcohol-induced decline.

Another two recent studies have investigated brain changes seen in people and animals with alcohol dependence. Each of these studies found a common culprit: inflamed microglia.

Microglia are the brains resident immune system cells. Their main role is to guard and maintain balance in the brain. When microglia detect a threat, they respond by becoming inflamed and attacking. Normally, they return to normal after the threat is gone, but sometimes when inflammation becomes uncontrollable such as with Alzeimers disease it can lead to brain degeneration.

One recent study used mice to study the effect of alcohol dependence on the brain.

In the brains of male mice that had alcohol dependency, research found there were more microglia cells in the medial prefrontal cortex, a region associated with pain, decision making, and memory processes. Similar results have also previously been found in humans.

They then examined what effects microglia depletion had on alcohol dependent mice by looking at their alcohol seeking behaviour, and anxious behaviour during alcohol withdrawal. The researchers found both factors were lowered when the microglia cells were reduced in the brain.

They also saw gene changes with microglia depletion. Genes involved in inflammation and immune responses were expressed less after depletion. The expression of genes involved in alcohol consumption, and alcohol dependence also changed when microglia had decreased. They also found that microglia depletion weakens brain circuits involved in the development of dependence and relapse behaviour in rodents.

A second study looking at both rodent and human brains also showed microglia is involved in alcohol dependence.

The researchers of this study used brain imaging, microglia depletion, and studies of post mortem brains, to examine changes that occur in alcohol dependence. For the brain imaging part, they used a variation of MRI scans, called DTI-MRI in humans and rats, focusing on a measure called mean diffusivity.

As DTI-MRI is based on the diffusion of water in tissues, mean diffusivity essentially shows the amount of diffusion of water molecules in tissues, with more dense and structurally-intact tissues having lower mean diffusivity. Mean diffusivity has previously been shown to change in the brain in inflammatory and degenerative conditions (including Alzheimers Disease and even psychosis). The researchers therefore chose to look at mean diffusivity as neuroinflammation is also involved in alcoholism. The researchers wanted to examine whether changes in mean diffusivity would be found between alcoholics and non-alcoholics, which hasnt been done before.

Indeed their findings showed that mean diffusivity is overall higher in the brain of alcohol dependent rats and humans. They also found additional changes in how certain neurotransmitters including dopamine, which is involved in alcohol dependence move and are distributed in the brain.

The researchers went on to examine the microglia in the brains of rats with alcohol dependence, and rats with previous dependence who had abstained from alcohol for a week. They found a decreased amount of microglia in specific brain regions of dependent rats (including the hippocampus, which is involved in memory, and the nucleus accumbens, which is involved in the reward system). The microglia in the brains of alcohol dependent rats were also in their inflamed form.

Although this study showed a decrease in microglia numbers whereas the previous study saw an increase this might be because the researchers looked at different brain regions and used different research methods and animal models. However, both studies give hints towards how microglia functions during alcohol consumption and dependence, may differ in different brain regions.

The researchers also found that depleting microglia from the brain, or inducing microglias inflammatory response, led to similar results to each other, as both increased the mean diffusivity. Changes in microglias form when inflamed were also similar to the ones they observed in dependent rats. They concluded that the changes in the brain areas they studied could be explained by an inflammatory reaction of microglia caused by alcohol.

One limitation of both studies findings is that they used both only male rodents and male humans. However, both studies exhibit how alcoholism is a complex disease that produces clear changes in the brain.

Examining how exactly microglia is involved, and being able to interfere with their responses, could lead to better understanding and detection of addiction to alcohol, and give a good stepping stone for future targeted interventions.

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Alcohol addiction: could the brain's immune system be the key to understanding and treating alcoholism? - The Conversation UK

It's the question everyone wants answered: How long are we protected from catching COVID-19 after we've recovered from the novel coronavirus?

Its the question everyone wants answered: How long are we protected from catching Covid-19 after weve recovered from the novel coronavirus and what does that really mean?

Last week, the US Centers for Disease Control and Prevention updated its quarantine guidelines online to say that people who have recovered from Covid-19 do not need to quarantine or get tested again for up to three months but the agency clarified in a statement to CNN on Friday that does not mean that people are immune to reinfection.

People who have tested positive for COVID-19 do not need to quarantine or get tested again for up to 3 months as long as they do not develop symptoms again, the CDC guidance stated.

A CDC spokesperson said the guidance is based on the latest science about COVID-19 showing that people can continue to test positive for up to 3 months after diagnosis and not be infectious to others.

Yet this science does not imply a person is immune to reinfection with SARS-CoV-2, the virus that causes COVID-19, in the 3 months following infection. The latest data simply suggests that retesting someone in the 3 months following initial infection is not necessary unless that person is exhibiting the symptoms of COVID-19 and the symptoms cannot be associated with another illness, the CDC statement said.

I think this is an incredibly sticky wicket, as the British would say, said Dr. William Schaffner, a professor of preventive medicine and infectious diseases at Vanderbilt University School of Medicine in Nashville, who was not involved in the CDC guidance.

We think antibodies correlate with protection, but we dont really know that yet, Schaffner said.

Practical applications, Schaffner added, are still a long way off. Can a person who has antibodies begin to date or stop wearing a mask, for example? Absolutely not, he said emphatically.

Our adaptive immune system, designed to target a specific and previously recognized invader, contains two main cellular components B cells and T cells. Studies on immunity so far have focused mainly on B cells, a type of white blood cell programmed to find and bind to foreign invaders.

Once it has attached itself to a virus such as the novel coronavirus that causes Covid-19, a B cell copies itself and churns out antibodies, eventually creating a mega-army of neutralizers for that particular invader, said CNN Chief Medical Correspondent Dr. Sanjay Gupta in an explainer on virus immunity.

Unfortunately, a few recent studies have found that antibodies to this particular coronavirus can fade away pretty quickly especially in people who have had mild cases of Covid-19, Gupta said.

A pre-print paper (meaning it has not been published in a peer-reviewed journal) released in July found antibody responses appear to decline 20 to 30 days after Covid-19 symptoms first appear.

This study has important implications when considering protection against re-infection with SARS-CoV-2 and the durability of vaccine protection, the researchers wrote in the paper.

In June, a small study found that people who have coronavirus infections but never develop symptoms could have weaker immune responses to the virus.

That study found that a group of about three dozen Covid-19 patients who were asymptomatic had levels of antibodies that were significantly lower than what was found among patients who had mild symptoms a finding that suggests the asymptomatic patients had weaker immune responses.

In early July, a Spanish government study found that just 5% of people in Spain have coronavirus antibodies and in a potentially worrying development, the study also indicated that peoples immunity to coronavirus wanes after just a few weeks. The findings show that 95% of Spains population remains susceptible to the virus.

This means that any perceived immunity can be incomplete, transitory and then disappear, said Dr. Raquel Yotti, head of the Carlos III Health Institute, in a news conference at the time. The institute is a key government agency leading the study.

Science is hoping that Covid-19 will also trigger an immune response from another arm of the adaptive immune system T cells. One type, called a memory T cell, helps the body remember a specific invader in case it comes back.

A recent study found such memory T cells in people infected with SARS-CoV-2, the novel coronavirus that creates the disease called Covid-19. That finding leads to speculation that some people might get milder cases of Covid-19 because their T-cells are reacting to exposure to similar coronaviruses encountered in the past.

The virus SARS-CoV-2 belongs to a large family of coronaviruses, six of which were previously known to infect humans. Two are deadly: SARS-CoV-1, the virus responsible for the outbreak of Severe Acute Respiratory Syndrome (SARS), which ended in 2004; and MERS-CoV, the virus that causes Middle East Respiratory Syndrome (MERS).

The other four cause the common cold, and because they circulate widely each year, its possible many people may have already been exposed to one of these so-called cousins of the novel coronavirus.

Theyve been studied and we know that after you had a cold, you develop antibodies to that particular human strain of coronavirus and you will be protected, but it turns out the protection begins to wane after about a year, Schaffner said.

Now when Covid-19 came along, we wondered how much protection are you going to get from this virus? And if you get protection, how long does it last? he added. We dont know that behavior yet.

Another page on the CDC site, updated in June, refers to the uncertainty that exists surrounding the role of antibodies in future infections.

Having antibodies to the virus that causes COVID-19 might provide protection from getting infected with the virus again. If it does, we do not know how much protection the antibodies might provide or how long this protection might last, the CDC says in regard to testing.

Until science knows more about how long immunity lasts, Schaffner advised staying the course of what is known to work: hand-washing, social distancing, avoiding crowds and wearing masks.

Dont go around looking for reasons not to wear the mask, just wear it. Get used to it, Schaffner said. We want to all be in this together to affirm our solidarity.

Editors note: This article has been updated to include comment from CDC clarifying its quarantine guidance.

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Are you immune to COVID-19 for three months after recovering? Its not clear - WTOP

Amid the pandemic, staying healthy is a top priority for most.

CLEVELAND As the state of Ohio continues it's fight against thecoronavirus pandemic, staying healthy seems to be a top priority for everyone.

But outside of washing your hands, not touching your face and proper social distancing, how can you increase your health and overall wellness? The Cleveland Clinic recommends boosting your immune system.

You diet can have a huge impact on your immune Health.

I believe in the power of immune-boosting foods, says Dr. Darling. Choosing whole, unprocessed foods does wonders for overall health, says Preventive medicine physician and wellness expert Sandra Darling.

She suggests adding foods like garlic, prebiotics, vitamin C-rich foods, and antioxidants to your diet to give your system a boost.

Listen, we know it's hard, but living under constant stress is detrimental to the body. Too much stress "cause causes the body to produce too much cortisol, the stress hormone. Over time, elevated cortisol lowers your resistance to fighting off infection and contributes to poor sleep and higher blood pressure," according to the clinic. Dr. Darling suggests making sure you get enough sleep, exercise and try meditation.

A little bit of positivity goes a long way. "Research shows that positive thoughts reduce stress and inflammation and increase resilience to infection while negative emotions can make you more susceptible to the common cold and flu," according to the Clinic.

If you've done all that you can when it comes to taking care of your immune system health, the Clinic recommends trying supplements and or essential oils.

The Clinic also recommends making sure you're taking time for yourself to rest in recharge. There's a lot going on in the world, you can't pour from an empty cup--so fill yours up!

For more information on the Clinic tips and resources, click here.

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Cleveland Clinic: Four ways to boost your immune health - WKYC.com