4 Tips To Boost Your Immune System During Cold & Flu Season | WUWM 89.7 FM

4 Tips To Boost Your Immune System During Cold & Flu Season | WUWM 89.7 FM

  • March 28, 2021

Cold and flu season is now upon us. That compounded with the ongoing coronavirus pandemic means it’s time to focus on our immune systems.  

Immune systems are pretty effective against many germs and viruses, but it takes time to fight them. And this year has added stress for many due to the many impacts of the coronavirus pandemic. “So, anything you can do to mitigate that stress by simple measures is going to be very helpful,” says Josh Knox, a physician assistant by training and a clinical associate professor at Marquette University’s physician assistant program.

Knox shares some tips to help strengthen your immune system this cold and flu season:

Sleep

Our bodies need sleep for our immune systems to work properly. “At night, besides your tired aching bones and muscles, your immune system is rebuilding while you’re sleeping,” Knox explains.

Our bodies also produce and release signaling proteins called cytokines that orchestrate our immune system while we sleep. T-cells are also produced at night, and Kox says “there’s also some evidence that those T-cells stick to their targets a little better when we get adequate sleep.”

The National Sleep Foundation recommends that adults sleep seven to nine hours a night to stay healthy. While not enough research has been conducted related to COVID-19, other research has shown that people sleeping six hours or less were more than four times more likely to catch other cold viruses. 

Exercise

People getting the recommended 150-300 minutes of moderate or vigorous aerobic exercise and two weight-like training sessions during the week helps antibody formations. Exercise also helps the body’s B-cells that make antibodies, according to Knox.  

“Normally, our white blood cells or those T-cells are kind of hanging out on the edge of our blood system, and exercise actually shocks them into activity and it turns them over more efficiently,” he explains.

Studies have also shown that people who exercise regularly are less susceptible to cold and flu-like viruses, and have reduced upper respiratory infections with shorter periods of being sick. “There is one study that shows that those individuals who are regularly exercising potentially can prevent or at least reduce the severity of severe reactions to COVID-19,” says Knox. 

Vitamin D

While there are plenty of vitamins to choose from over the counter, “there’s probably only one supplement that has enough data to say something intelligent about it at this time — and that is vitamin D,” says Knox.

Vitamin D helps regulate calcium and phosphate to keep bones, teeth and muscles healthy. Knox notes that the best way to get it is through sunshine and healthy meals, but taking supplements can help your immune function as well. 

“There is reams of data from other viruses and other upper respiratory infections that suggest that individuals are less susceptible to cold viruses and upper respiratory viruses when they have adequate vitamin D,” says Knox.

When it comes to the coronavirus, a study has shown that people will have a less severe case and have a lower risk of death when they have enough vitamin D, according to Knox. 

Get the flu shot

In addition to getting good sleep, exercising, and getting enough vitamin D, Knox says that getting the flu shot this year “is more important than ever.”

He notes that people could be weakened by getting the flu and become more susceptible to COVID-19 or need to be hospitalized with the flu and risk further exposure to the coronavirus.  

“The flu vaccine does not cause the flu,” states Knox. “Very few people have adverse reactions to it, beyond very mild ones, and I think it’s essential for everybody to get it this year.”

Children's immune response more effective against COVID-19 -- ScienceDaily

Repurposed heart and flu drugs may help body fight sepsis — ScienceDaily

  • March 27, 2021

Despite continued improvements in antibiotics and hospital intensive care, staph sepsis — a bloodstream infection caused by Staphylococcus aureus bacteria — still causes severe illness or death in 20 to 30 percent of patients who contract it.

Rather than continue to throw more antibiotics at the problem, University of California San Diego researchers want to boost the other side of the equation: the patient’s own immune system.

The team recently discovered a battle that occurs between staph bacteria and platelets — blood cells known better for their role in clotting than in immune defense. In some sepsis cases, they found, the bacteria win out and platelet levels plummet. Patients with fewer platelets were more likely to die of staph sepsis than patients with higher platelet counts.

The researchers also determined that two currently available prescription medications, approved by the U.S. Food and Drug Administration (FDA) for other uses, protect platelets and improve survival in mouse models of staph sepsis. The two repurposed drugs were ticagrelor (Brilinta), a blood thinner commonly prescribed to prevent heart attack recurrence, and oseltamivir (Tamiflu), prescribed to treat the flu.

The study publishes March 24, 2021 in Science Translational Medicine.

“In many cases, the antibiotics we give these patients should be able to kill the bacteria, based on lab tests, yet a significant number of patients are not pulling through,” said senior author Victor Nizet, MD, Distinguished Professor at UC San Diego School of Medicine and Skaggs School of Pharmacy and Pharmaceutical Sciences. “If we can reduce mortality in staph sepsis by 10 or 20 percent by arming or protecting the immune system, we can likely save more lives than discovering an additional new antibiotic that may still not cure the sickest patients.”

The study started with a group of 49 University of Wisconsin patients with staph sepsis. The team collected the patients’ blood, bacteria samples, and demographic and health information. To their surprise, it wasn’t white blood cell counts (immune cells) that correlated with patient outcomes — it was the platelet count. Low platelet counts, defined in this case as fewer than 100,000 per mm3 blood, were associated with increased risk of death from staph sepsis. Approximately 31 percent of patients with low platelet counts died from the infection, compared to less than 6 percent of patients with platelets above the threshold.

In laboratory experiments, the researchers worked out what’s likely happening: Platelets secrete antimicrobial peptides that help the immune system destroy staph bacteria. At the same time, staph release an alpha-toxin that’s detrimental to platelets. In addition to poking holes in platelets, the bacteria’s alpha-toxin convinces the blood cells to produce an enzyme that trims off sugar molecules that decorate their own surfaces. The platelet’s new look is recognized by another molecule in the liver called the Ashwell-Morell receptor, which pulls “bald” platelets out of circulation.

Once Nizet and team had an idea of what might be happening in the patients who are less likely to survive staph sepsis, they turned to mouse models of the disease to find ways to tip the balance of what they call the “toxin-platelet-receptor” axis back in favor of the human patient.

The researchers tested several classes of drugs known to be safe in humans and known to act on platelets. Most drugs they tested had no effect, but two drugs made a big difference. Ticagrelor blocks staph’s alpha-toxin so it can’t injure platelets or stimulate its sugar-removing enzyme. Oseltamivir inhibits the platelet sugar-removing enzyme so the cells don’t go bald and aren’t cleared by the liver, even when staph’s alpha-toxin is around.

Mice with staph sepsis and treated with either ticagrelor or oseltamivir maintained more platelets and had less bacteria in their blood. Ultimately, approximately 60 percent of treated mice survived 10 days following infection, compared to 20 percent of untreated mice.

Side effects of these medications may include nausea, diarrhea and nosebleeds, and ticagrelor may cause uncontrollable bleeding. While new clinical trials specifically designed to test the drugs’ safety and efficacy for patients with staph sepsis would be ideal, Nizet said there’s little financial incentive for pharmaceutical companies to do so with an already profitable drug.

Still, repurposing commercially available drugs has many advantages.

“Discovering a new drug is tremendously expensive and takes many, many years,” said Nizet, who is also faculty lead for the Collaborative to Halt Antibiotic-Resistant Microbes (CHARM) at UC San Diego. “But if we look around at what we already have, what we already know to be safe, we may find many opportunities to improve patient outcomes.”

Sepsis can be caused by several types of bacteria in addition to staph, including Streptococcus pyogenes, Klebsiella, E. coli and Pseudomonas aeruginosa. According to the Centers for Disease Control and Prevention, each year at least 1.7 million adults in the U.S. develop sepsis and nearly 270,000 die as a result. One in three patients who die in a hospital has sepsis. And it’s one of the costliest of all diseases — in 2013, for example, the Department of Health and Human Services reported that sepsis management added up to more than $24 billion in hospital expenses, or 13 percent of total U.S. hospital costs.

Repurposed heart and flu drugs that protect platelets improve survival of septic mice

Repurposed heart and flu drugs that protect platelets improve survival of septic mice

  • March 25, 2021

Despite continued improvements in antibiotics and hospital intensive care, staph sepsis -; a bloodstream infection caused by Staphylococcus aureus bacteria -; still causes severe illness or death in 20 to 30 percent of patients who contract it.

Rather than continue to throw more antibiotics at the problem, University of California San Diego researchers want to boost the other side of the equation: the patient’s own immune system.

The team recently discovered a battle that occurs between staph bacteria and platelets -; blood cells known better for their role in clotting than in immune defense. In some sepsis cases, they found, the bacteria win out and platelet levels plummet. Patients with fewer platelets were more likely to die of staph sepsis than patients with higher platelet counts.

The researchers also determined that two currently available prescription medications, approved by the U.S. Food and Drug Administration (FDA) for other uses, protect platelets and improve survival in mouse models of staph sepsis. The two repurposed drugs were ticagrelor (Brilinta), a blood thinner commonly prescribed to prevent heart attack recurrence, and oseltamivir (Tamiflu), prescribed to treat the flu.

The study publishes March 24, 2021 in Science Translational Medicine.

In many cases, the antibiotics we give these patients should be able to kill the bacteria, based on lab tests, yet a significant number of patients are not pulling through. If we can reduce mortality in staph sepsis by 10 or 20 percent by arming or protecting the immune system, we can likely save more lives than discovering an additional new antibiotic that may still not cure the sickest patients.”


Victor Nizet, MD, Senior Author, Distinguished Professor at UC San Diego School of Medicine and Skaggs School of Pharmacy and Pharmaceutical Sciences

The study started with a group of 49 University of Wisconsin patients with staph sepsis. The team collected the patients’ blood, bacteria samples, and demographic and health information. To their surprise, it wasn’t white blood cell counts (immune cells) that correlated with patient outcomes -; it was the platelet count. Low platelet counts, defined in this case as fewer than 100,000 per mm3 blood, were associated with increased risk of death from staph sepsis. Approximately 31 percent of patients with low platelet counts died from the infection, compared to less than 6 percent of patients with platelets above the threshold.

In laboratory experiments, the researchers worked out what’s likely happening: Platelets secrete antimicrobial peptides that help the immune system destroy staph bacteria. At the same time, staph release an alpha-toxin that’s detrimental to platelets. In addition to poking holes in platelets, the bacteria’s alpha-toxin convinces the blood cells to produce an enzyme that trims off sugar molecules that decorate their own surfaces. The platelet’s new look is recognized by another molecule in the liver called the Ashwell-Morell receptor, which pulls “bald” platelets out of circulation.

Once Nizet and team had an idea of what might be happening in the patients who are less likely to survive staph sepsis, they turned to mouse models of the disease to find ways to tip the balance of what they call the “toxin-platelet-receptor” axis back in favor of the human patient.

The researchers tested several classes of drugs known to be safe in humans and known to act on platelets. Most drugs they tested had no effect, but two drugs made a big difference. Ticagrelor blocks staph’s alpha-toxin so it can’t injure platelets or stimulate its sugar-removing enzyme. Oseltamivir inhibits the platelet sugar-removing enzyme so the cells don’t go bald and aren’t cleared by the liver, even when staph’s alpha-toxin is around.

Mice with staph sepsis and treated with either ticagrelor or oseltamivir maintained more platelets and had less bacteria in their blood. Ultimately, approximately 60 percent of treated mice survived 10 days following infection, compared to 20 percent of untreated mice.

Side effects of these medications may include nausea, diarrhea and nosebleeds, and ticagrelor may cause uncontrollable bleeding. While new clinical trials specifically designed to test the drugs’ safety and efficacy for patients with staph sepsis would be ideal, Nizet said there’s little financial incentive for pharmaceutical companies to do so with an already profitable drug.

Still, repurposing commercially available drugs has many advantages.

“Discovering a new drug is tremendously expensive and takes many, many years,” said Nizet, who is also faculty lead for the Collaborative to Halt Antibiotic-Resistant Microbes (CHARM) at UC San Diego. “But if we look around at what we already have, what we already know to be safe, we may find many opportunities to improve patient outcomes.”

Sepsis can be caused by several types of bacteria in addition to staph, including Streptococcus pyogenes, Klebsiella, E. coli and Pseudomonas aeruginosa. According to the Centers for Disease Control and Prevention, each year at least 1.7 million adults in the U.S. develop sepsis and nearly 270,000 die as a result. One in three patients who die in a hospital has sepsis. And it’s one of the costliest of all diseases -; in 2013, for example, the Department of Health and Human Services reported that sepsis management added up to more than $24 billion in hospital expenses, or 13 percent of total U.S. hospital costs.

Source:

Journal reference:

Sun, J., et al. (2021) Repurposed drugs block toxin-driven platelet clearance by the hepatic Ashwell-Morell receptor to clear Staphylococcus aureus bacteremia. Science Translational Medicine. doi.org/10.1126/scitranslmed.abd6737.

Repurposed Heart and Flu Drugs May Help Body Fight Sepsis

Repurposed Heart and Flu Drugs May Help Body Fight Sepsis

  • March 24, 2021

Despite continued improvements in antibiotics and hospital intensive care, staph sepsis — a bloodstream infection caused by Staphylococcus aureus bacteria — still causes severe illness or death in 20 to 30 percent of patients who contract it.

Rather than continue to throw more antibiotics at the problem, University of California San Diego researchers want to boost the other side of the equation: the patient’s own immune system.

The team recently discovered a battle that occurs between staph bacteria and platelets — blood cells known better for their role in clotting than in immune defense. In some sepsis cases, they found, the bacteria win out and platelet levels plummet. Patients with fewer platelets were more likely to die of staph sepsis than patients with higher platelet counts.

The researchers also determined that two currently available prescription medications, approved by the U.S. Food and Drug Administration (FDA) for other uses, protect platelets and improve survival in mouse models of staph sepsis. The two repurposed drugs were ticagrelor (Brilinta), a blood thinner commonly prescribed to prevent heart attack recurrence, and oseltamivir (Tamiflu), prescribed to treat the flu.

The study is published March 24, 2021 in Science Translational Medicine.

“In many cases, the antibiotics we give these patients should be able to kill the bacteria, based on lab tests, yet a significant number of patients are not pulling through,” said senior author Victor Nizet, MD, Distinguished Professor at UC San Diego School of Medicine and Skaggs School of Pharmacy and Pharmaceutical Sciences. “If we can reduce mortality in staph sepsis by 10 or 20 percent by arming or protecting the immune system, we can likely save more lives than discovering an additional new antibiotic that may still not cure the sickest patients.”

platelets

Left: Human platelets are destroyed by Staphylococcus aureus bacteria (circles). Right: With the addition of blood thinner ticagrelor, human platelets (larger blobs) are protected from injury by Staphylococcus aureus (smaller circles).

The study started with a group of 49 University of Wisconsin patients with staph sepsis. The team collected the patients’ blood, bacteria samples, and demographic and health information. To their surprise, it wasn’t white blood cell counts (immune cells) that correlated with patient outcomes — it was the platelet count. Low platelet counts, defined in this case as fewer than 100,000 per mm3 blood, were associated with increased risk of death from staph sepsis. Approximately 31 percent of patients with low platelet counts died from the infection, compared to less than 6 percent of patients with platelets above the threshold.

In laboratory experiments, the researchers worked out what’s likely happening: Platelets secrete antimicrobial peptides that help the immune system destroy staph bacteria. At the same time, staph release an alpha-toxin that’s detrimental to platelets. In addition to poking holes in platelets, the bacteria’s alpha-toxin convinces the blood cells to produce an enzyme that trims off sugar molecules that decorate their own surfaces. The platelet’s new look is recognized by another molecule in the liver called the Ashwell-Morell receptor, which pulls “bald” platelets out of circulation.

Once Nizet and team had an idea of what might be happening in the patients who are less likely to survive staph sepsis, they turned to mouse models of the disease to find ways to tip the balance of what they call the “toxin-platelet-receptor” axis back in favor of the human patient.

The researchers tested several classes of drugs known to be safe in humans and known to act on platelets. Most drugs they tested had no effect, but two drugs made a big difference. Ticagrelor blocks staph’s alpha-toxin so it can’t injure platelets or stimulate its sugar-removing enzyme. Oseltamivir inhibits the platelet sugar-removing enzyme so the cells don’t go bald and aren’t cleared by the liver, even when staph’s alpha-toxin is around.

Mice with staph sepsis and treated with either ticagrelor or oseltamivir maintained more platelets and had less bacteria in their blood. Ultimately, approximately 60 percent of treated mice survived 10 days following infection, compared to 20 percent of untreated mice.

Side effects of these medications may include nausea, diarrhea and nosebleeds, and ticagrelor may cause uncontrollable bleeding. While new clinical trials specifically designed to test the drugs’ safety and efficacy for patients with staph sepsis would be ideal, Nizet said there’s little financial incentive for pharmaceutical companies to do so with an already profitable drug.

Still, repurposing commercially available drugs has many advantages.

“Discovering a new drug is tremendously expensive and takes many, many years,” said Nizet, who is also faculty lead for the Collaborative to Halt Antibiotic-Resistant Microbes (CHARM) at UC San Diego. “But if we look around at what we already have, what we already know to be safe, we may find many opportunities to improve patient outcomes.”

Sepsis can be caused by several types of bacteria in addition to staph, including Streptococcus pyogenes, Klebsiella, E. coli and Pseudomonas aeruginosa. According to the Centers for Disease Control and Prevention, each year at least 1.7 million adults in the U.S. develop sepsis and nearly 270,000 die as a result. One in three patients who die in a hospital has sepsis. And it’s one of the costliest of all diseases — in 2013, for example, the Department of Health and Human Services reported that sepsis management added up to more than $24 billion in hospital expenses, or 13 percent of total U.S. hospital costs.

Co-authors of the study include: Josh Sun, Satoshi Uchiyama, Joshua Olson, Ingrid Cornax, Nao Ando, Yohei Kohno, May M. T. Kyaw, Bernice Aguilar, Nina M. Haste, George Sakoulas, UC San Diego; Yosuke Morodomi, Sachiko Kanaji, Taisuke Kanaji, Scripps Research; Warren E. Rose, University of Wisconsin; and Jamey D. Marth, UC Santa Barbara and Sanford Burnham Prebys Medical Discovery Institute.

Funding for this research came, in part, from the National Institutes of Health (grants HL125352, HL107150, HL131474, AI124326, HD090259, AI13262 and OD017863) and the UC San Diego PharmD/PhD Program.

Disclosure: Warren Rose has received speaking honoraria from Melinta unrelated to the current study. George Sakoulas has consulted for Allergan, Paratek, and Octapharma unrelated to the current study. Victor Nizet has consulted for Cellics Therapeutics, Staurus, Vaxcyte, Clarametyx Biosciences, SNIPR Biome, Boehringer Ingelheim, and Iogen unrelated to the current study.


watercolor illustration of coronavirus cells

Coronavirus Deranges the Immune System in Complex and Deadly Ways

  • March 4, 2021


This story also ran on USA Today. It can be republished for free.

There’s a reason soldiers go through basic training before heading into combat: Without careful instruction, green recruits armed with powerful weapons could be as dangerous to one another as to the enemy.

The immune system works much the same way. Immune cells, which protect the body from infections, need to be “educated” to recognize bad guys — and to hold their fire around civilians.

In some covid patients, this education may be cut short. Scientists say unprepared immune cells appear to be responding to the coronavirus with a devastating release of chemicals, inflicting damage that may endure long after the threat has been eliminated.

“If you have a brand-new virus and the virus is winning, the immune system may go into an ‘all hands on deck’ response,” said Dr. Nina Luning Prak, co-author of a January study on covid and the immune system. “Things that are normally kept in close check are relaxed. The body may say, ‘Who cares? Give me all you’ve got.’”

While all viruses find ways to evade the body’s defenses, a growing field of research suggests that the coronavirus unhinges the immune system more profoundly than previously realized.

Some covid survivors have developed serious autoimmune diseases, which occur when an overactive immune system attacks the patient, rather than the virus. Doctors in Italy first noticed a pattern in March 2020, when several covid patients developed Guillain-Barré syndrome, in which the immune systems attacks nerves throughout the body, causing muscle weakness or paralysis. As the pandemic has surged around the world, doctors have diagnosed patients with rare, immune-related bleeding disorders. Other patients have developed the opposite problem, suffering blood clots that can lead to stroke.

All these conditions can be triggered by “autoantibodies” — rogue antibodies that target the patient’s own proteins and cells.

In a report published in October, researchers even labeled the coronavirus “the autoimmune virus.”

“Covid is deranging the immune system,” said John Wherry, director of the Penn Medicine Immune Health Institute and another co-author of the January study. “Some patients, from their very first visit, seem to have an immune system in hyperdrive.”

Although doctors are researching ways to overcome immune disorders in covid patients, new treatments will take time to develop. Scientists are still trying to understand why some immune cells become hyperactive — and why some refuse to stand down when the battle is over.

Key immune players called “helper T cells” typically help antibodies mature. If the body is invaded by a pathogen, however, these T cells can switch jobs to hunt down viruses, acting more like “killer T cells,” which destroy infected cells. When an infection is over, helper T cells usually go back to their old jobs.

In some people with severe covid, however, helper T cells don’t stand down when the infection is over, said James Heath, a professor and president of Seattle’s Institute for Systems Biology.

About 10% to 15% of hospitalized covid patients Heath studied had high levels of these cells even after clearing the infection. By comparison, Heath found lingering helper T cells in fewer than 5% of covid patients with less serious infections.

In affected patients, helper T cells were still looking for the enemy long after it had been eliminated. Heath is now studying whether these overzealous T cells might inflict damage that leads to chronic illness or symptoms of autoimmune disease.

“These T cells are still there months later and they’re aggressive,” Heath said. “They’re on the hunt.”

Friendly Fire

Covid appears to confuse multiple parts of the immune system.

In some patients, covid triggers autoantibodies that target the immune system itself, leaving patients without a key defense against the coronavirus.

In October, a study published in Science led by Rockefeller University’s Jean-Laurent Casanova showed that about 10% of covid patients become severely ill because they have antibodies against an immune system protein called interferon.

Disabling interferon is like knocking down a castle’s gate. Without these essential proteins, invading viruses can overwhelm the body and multiply wildly.

New research shows that the coronavirus may activate preexisting autoantibodies, as well as prompt the body to make new ones.

In the January study, half of the hospitalized covid patients had autoantibodies, compared with fewer than 15% of healthy people. While some of the autoantibodies were present before patients were infected with SARS-CoV-2, others developed over the course of the illness.

Other research has produced similar findings. In a study out in December, researchers found that hospitalized covid patients harbored a diverse array of autoantibodies.

While some patients studied had antibodies against virus-fighting interferons, others had antibodies that targeted the brain, thyroid, blood vessels, central nervous system, platelets, kidneys, heart and liver, said Dr. Aaron Ring, assistant professor of immunology at Yale School of Medicine and lead author of the December study, published online without peer review. Some patients had antibodies associated with lupus, a chronic autoimmune disorder that can cause pain and inflammation in any part of the body.

In his study, Ring and his colleagues found autoantibodies against proteins that help coordinate the immune system response. “These are the air traffic controllers,” Ring said. If these proteins are disrupted, “your immune system doesn’t work properly.”

Covid patients rife with autoantibodies tended to have the severest disease, said Ring, who said he was surprised at the level of autoantibodies in some patients. “They were comparable or even worse than lupus,” Ring said.

Although the studies are intriguing, they don’t prove that autoantibodies made people sicker, said Dr. Angela Rasmussen, a virologist affiliated with Georgetown’s Center for Global Health Science and Security. It’s possible that the autoantibodies are simply markers of serious disease.

“It’s not clear that this is linked to disease severity,” Rasmussen said.

The studies’ authors acknowledge they have many unanswered questions.

“We don’t yet know what these autoantibodies do and we don’t know if [patients] will go on to develop autoimmune disease,” said Dr. PJ Utz, a professor of immunology and rheumatology at Stanford University School of Medicine and a co-author of Luning Prak’s paper.

But recent discoveries about autoantibodies have excited the scientific community, who now wonder if rogue antibodies could explain patients’ differing responses to many other viruses. Scientists also want to know precisely how the coronavirus turns the body against itself — and how long autoantibodies remain in the blood.

‘An Unfortunate Legacy’

Scientists working round-the-clock are already beginning to unravel these mysteries.

A study published online in January, for example, found rogue antibodies in patients’ blood up to seven months after infection.

Ring said researchers would like to know if lingering autoantibodies contribute to the symptoms of “long covid,” which afflicts one-third of covid survivors up to nine months after infection, according to a new study in JAMA Network Open.

“Long haulers” suffer from a wide range of symptoms, including debilitating fatigue, shortness of breath, cough, chest pain and joint pain, according to the Centers for Disease Control and Prevention. Other patients experience depression, muscle pain, headaches, intermittent fevers, heart palpitations and problems with concentration and memory, known as brain fog.

Less commonly, some patients develop an inflammation of the heart muscle, abnormalities in their lung function, kidney issues, rashes, hair loss, smell and taste problems, sleep issues and anxiety.

The National Institutes of Health has announced a four-year initiative to better understand long covid, using $1.15 billion allocated by Congress.

Ring said he’d like to study patients over time to see if specific symptoms might be explained by lingering autoantibodies.

“We need to look at the same patients a half-year later and see which antibodies they do or don’t have,” he said. If autoantibodies are to blame for long covid, they could “represent an unfortunate legacy after the virus is gone.”

Widening the Investigation

Scientists say the coronavirus could undermine the immune system in several ways.

For example, it’s possible that immune cells become confused because some viral proteins resemble proteins found on human cells, Luning Prak said. It’s also possible that the coronavirus lurks in the body at very low levels even after patients recover from their initial infection.

“We’re still at the very beginning stages of this,” said Luning Prak, director of Penn Medicine’s Human Immunology Core Facility.

Dr. Shiv Pillai, a Harvard Medical School professor, notes that autoantibodies aren’t uncommon. Many healthy people walk around with dormant autoantibodies that never cause harm.

For reasons scientists don’t completely understand, viral infections appear able to tip the scales, triggering autoantibodies to attack, said Dr. Judith James, vice president of clinical affairs at the Oklahoma Medical Research Foundation and a co-author of Luning Prak’s study.

For example, the Epstein-Barr virus, best known for causing mononucleosis, has been linked to lupus and other autoimmune diseases. The bacteria that cause strep throat can lead to rheumatic fever, an inflammatory disease that can cause permanent heart damage. Doctors also know that influenza can trigger an autoimmune blood-clotting disorder, called thrombocytopenia.

Researchers are now investigating whether autoantibodies are involved in other illnesses — a possibility scientists rarely considered in the past.

Doctors have long wondered, for example, why a small number of people — mostly older adults — develop serious, even life-threatening reactions to the yellow fever vaccine. Three or four out of every 1 million people who receive this vaccine — made with a live, weakened virus — develop yellow fever because their immune systems don’t respond as expected, and the weakened virus multiplies and causes disease.

In a new paper in the Journal of Experimental Medicine, Rockefeller University’s Casanova has found that autoantibodies to interferon are once again to blame.

Casanova led a team that found three of the eight patients studied who experienced a dangerous vaccine reaction had autoantibodies that disabled interferon. Two other patients in the study had genes that disabled interferon.

“If you have these autoantibodies and you are vaccinated against yellow fever, you may end up in the ICU,” Casanova said.

Casanova’s lab is now investigating whether autoantibodies cause critical illness from influenza or herpes simplex virus, which can cause a rare brain inflammation called encephalitis.

Calming the Autoimmune Storm

Researchers are looking for ways to treat patients who have interferon deficiencies — a group at risk for severe covid complications.

In a small study published in February in the Lancet Respiratory Medicine, doctors tested an injectable type of interferon — called peginterferon-lambda — in patients with early covid infections.

People randomly assigned to receive an interferon injection were four times more likely to have cleared their infections within seven days than the placebo group. The treatment, which used a type of interferon not targeted by the autoantibodies Casanova discovered, had the most dramatic benefits in patients with the highest viral loads.

Lowering the amount of virus in a patient may help them avoid becoming seriously ill, said Dr. Jordan Feld, lead author of the 60-person study and research director at the Toronto Centre for Liver Disease in Canada. In his study, four of the placebo patients went to the emergency room because of breathing issues, compared with only one who received interferon.

“If we can bring the viral levels down quickly, they might be less infectious,” Feld said.

Feld, a liver specialist, notes that doctors have long studied this type of interferon to treat other viral infections, such as hepatitis. This type of interferon causes fewer side effects than other varieties. In the trial, those treated with interferon had similar side effects to those who received a placebo.

Doctors could potentially treat patients with a single injection with a small needle — like those used to administer insulin — in outpatient clinics, Feld said. That would make treatment much easier to administer than other therapies for covid, which require patients to receive lengthy infusions in specialized settings.

Many questions remain. Dr. Nathan Peiffer-Smadja, a researcher at the Imperial College London, said it’s unclear whether this type of interferon does improve symptoms.

Similar studies have failed to show any benefit to treating patients with interferon, and Feld acknowledged that his results need to be confirmed in a larger study. Ideally, Feld said, he would like to test interferon in older patients to see whether it can reduce hospitalizations.

“We’d like to look at long haulers, to see if clearing the virus quickly could lead to less immune dysregulation,” Feld said. “People have said to me, ‘Do we really need new treatments now that vaccines are rolling out?’ Unfortunately, we do.”

Kaiser Health News (KHN) is a national health policy news service. It is an editorially independent program of the Henry J. Kaiser Family Foundation which is not affiliated with Kaiser Permanente.

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Here's How the COVID-19 Vaccines Stack Up Against the Flu Vaccine

Here’s How the COVID-19 Vaccines Stack Up Against the Flu Vaccine

  • February 8, 2021

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Long wines for COVID-19 vaccines have become commonplace in the U.S. Michael M. Santiago/Getty Images
  • Though the coronavirus vaccines and flu shots use distinctly different technologies against two unique viruses, they still have the same job of teaching our immune system how to recognize and attack a virus.
  • The COVID-19 shots appear to be even more effective at preventing severe disease, along with hospitalization and death.
  • Experts suspect the vaccine technologies developed during the pandemic will be used to improve existing vaccines such as the flu shot.

As of Feb. 8, more than 42 million doses of the Pfizer and Moderna COVID-19 vaccines have been administered in the United States.

The shots are safe, highly effective, and in most cases, cause mild reactions similar to the flu shot.

But, comparing the coronavirus vaccines to the flu shot is like comparing apples to oranges.

For one, the technologies used in the flu and coronavirus shots are significantly different. The viruses also have different attack rates and behavioral patterns.

And though both viruses mutate, the flu virus does so much more frequently, making it difficult to design and distribute a shot that can work perfectly against the leading flu strains each year.

Even so, both sets of shots are proficient at preventing severe illness and death.

Here’s how the COVID-19 shots stack up against the flu shot:

Though the coronavirus vaccines and flu shots use distinctly different technologies against two unique viruses, they still, on a basic level, have the same job.

The shots “provide an opportunity for the immune response to recognize a foreign protein or antigen,” explained Litjen Tan, PhD, the chief strategy officer of the Immunization Action Coalition.

These vaccines’ goal is to give the immune system a way to recognize a foreign pathogen and develop a memory response. If and when the body is exposed to the virus, the immune response can be activated faster.

This quick activation of the immune system can either prevent illness or reduce the severity of the disease to varying degrees.

“How you give the opportunity to the immune response to look at this foreign antigen varies [with each type of vaccine],” Tan said.

New data on the Moderna and Pfizer novel coronavirus shots show that most people experience mild reactions after being vaccinated, particularly after the second dose.

These reactions commonly include pain at the injection site and fatigue, headache, myalgia, and chills.

The flu shot is also known to trigger similar side effects — sore arm, a low-grade fever, headache, fatigue, and muscle aches.

According to Tan, the reactions are the same, but the effects reported after the coronavirus vaccines seem more intense.

“The side effects from COVID-19 vaccines are a little bit stronger. It’s a more reactive vaccine than flu vaccine,” he said.

In both cases, the side effects are a result of the immune system revving up and learning how to fight an infection.

The flu shots’ effectiveness fluctuates every year depending on how precisely the shots match the circulating strains, but health experts estimate it ranges from 40 to 60 percent, depending on the season.

Tan says researchers don’t conduct clinical trials on the flu shots anymore, so any recent evidence on the flu shot’s efficacy comes from looking at flu activity trends in the population.

That data suggests that “influenza vaccine not only prevents 40 to 60 against primary disease, but it’s also around that same level in terms of preventing hospitalization and severe illness in both kids and adults,” Tan said.

A study published in Pediatrics in 2017 found that the flu vaccine cuts the risk of death in healthy children by about two-thirds, or 65 percent.

And according to the Centers for Disease Control and Prevention (CDC), a person hospitalized with influenza is 2 to 5 times more likely to die if they’re unvaccinated.

Even when the flu vaccine isn’t a strong match against the circulating strains, it still confers some degree of protection.

“The greatest benefit is probably reducing the likelihood of someone getting severe influenza, reducing duration of flu symptoms, and limiting spread to others,” said Dr. David Hirschwerk, an attending infectious diseases physician at Northwell Health in Manhasset, New York.

The coronavirus vaccines range from about 66 to 95 percent effective at preventing symptomatic disease. All of the vaccines appear to be 100 percent effective at protecting people against hospitalization and death.

“The COVID vaccines, so far, have turned out to be more effective than the flu vaccine, not only in actually preventing COVID but notably in limiting cases of severe COVID,” Hirschwerk said.

Emerging evidence suggests efficacy may wane against certain variants.

“We already know that the variant from the UK is a bit less responsive to the vaccine, but it remains very likely that severe COVID can still be mitigated by the current vaccines and even if not perfect, that would remain a substantial victory for public health,” Hirschwerk said.

Many of the vaccine developers are already working on booster shots that specifically target emerging variants.

The ease with which the shots can be modified is one of the key benefits of the new technologies used in the COVID-19 vaccines.

Modifying vaccines is much harder with the traditional technologies used.

“It’s very hard to react and make changes to variations. We struggle with it every year with flu,” Tan said.

According to Tan, scientists evaluate a vaccine’s ability to prevent transmission by looking at the amount of virus in people who’ve been vaccinated.

“The general feeling with flu vaccine is that it does prevent transmission,” Tan said.

That said, even though it’s thought the flu shot can significantly reduce disease transmission, vaccinated people can still contact influenza and spread it to others.

There’s limited data looking at the new coronavirus vaccines’ ability to reduce transmission of COVID-19. One small study from AstraZeneca suggests it may cut the spread by up to 67 percent.

When looking at these vaccines’ ability to curb disease transmission, it’s important to understand that the flu and new coronavirus have different attack rates, Tan says.

COVID-19 has very high attack rates. There are a lot of people who are susceptible because there’s little natural immunity in the population. Also, there’s no widespread vaccination against COVID-19, and there are no antivirals.

With flu, we can reduce transmission with vaccination because there’s a lot of pre-existing immunity in the population. We also have effective influenza antivirals that can lessen the severity of illness, Tan says.

“A lot of people have been exposed to actual flu in the past or have been multiply vaccinated, and every time we vaccinate, we boost [immunity],” he said.

The attack rate of flu compared to COVID-19 is much lower. “The bar is very different,” Tan said.

Tan thinks the vaccination advancements we’ve made during the pandemic will be used to create new vaccines against many other conditions.

The technology could help make existing vaccines, like the flu shot, even better.

“I’m really optimistic that we’re going to see some genuine improvements in flu vaccine as a result of our COVID-19 technology,” Tan said.

Though the coronavirus vaccines and flu shots use distinctly different technologies against two unique viruses, they still, on a basic level, have the same job of teaching our immune system how to recognize and attack a virus. Both sets of shots trigger side effects that include fatigue, chills, and in some cases, a low grade fever. The COVID-19 shots appear to be even more effective at preventing severe disease, along with hospitalization and death. Health experts suspect the vaccine technologies developed during the pandemic will be used to improve existing vaccines such as the flu shot.

Like Flu, COVID-19 May Turn Out to Be Seasonal

Like Flu, COVID-19 May Turn Out to Be Seasonal

  • February 3, 2021

TUESDAY, Feb. 2, 2021 (HealthDay News) — Like influenza, could COVID-19 evolve to wax and wane with the seasons? New research suggests it might.

Early in the pandemic, some experts suggested that SARS-CoV-2 — the virus that causes COVID-19 — may behave like many other coronaviruses that circulate more widely in fall and winter.

To find out if that could be true, researchers analyzed COVID-19 data — including cases, death rates, recoveries, testing rates and hospitalizations — from 221 countries. The investigators found a strong association with temperature and latitude.

“One conclusion is that the disease may be seasonal, like the flu. This is very relevant to what we should expect from now on after the vaccine controls these first waves of COVID-19,” said senior study author Gustavo Caetano-Anollés. He is a professor at the C.R. Woese Institute for Genomic Biology at the University of Illinois at Urbana-Champaign.

The same research team previously identified areas in the SARS-CoV-2 virus genome undergoing rapid mutation.

Similar viruses have seasonal increases in mutation rates, so the researchers looked for connections between mutations in SARS-CoV-2 and temperature, latitude and longitude.

“Our results suggest the virus is changing at its own pace, and mutations are affected by factors other than temperature or latitude. We don’t know exactly what those factors are, but we can now say seasonal effects are independent of the genetic makeup of the virus,” Caetano-Anollés said in a university news release.

Further research is needed to learn more about how climate and different seasons may affect COVID-19 rates, the team added.

The study authors suggested that people’s immune systems may play a role. The immune system can be influenced by temperature and nutrition, including vitamin D, which plays an important role in immunity. With less sun exposure during the winter, most people don’t make enough vitamin D.

“We know the flu is seasonal, and that we get a break during the summer. That gives us a chance to build the flu vaccine for the following fall,” Caetano-Anollés said. “When we are still in the midst of a raging pandemic, that break is nonexistent. Perhaps learning how to boost our immune system could help combat the disease as we struggle to catch up with the ever-changing coronavirus.”

The study was published online Jan. 26 in the journal Evolutionary Bioinformatics.


More information

The U.S. Centers for Disease Control and Prevention has more on COVID-19.


SOURCE: University of Illinois at Urbana-Champaign, news release, Jan. 27, 2021

How to Stay Healthy During Cold and Flu Season: Tips

How to Stay Healthy During Cold and Flu Season: Tips

  • February 1, 2021
Stay Healthy and Pretty Through Cold and Flu Season
Shutterstock

Winter is here! While we love sipping hot cocoa by a crackling fire, we strongly dislike that along with cozy vibes, the chilly weather also ushers in cold and flu season. Fear not! We spoke with a top doctor and wellness expert to get tips that will take the guesswork out of how you can stay healthy during these months.

First, some good news. Because of the measures we’ve been taking to minimize the spread of Covid-19, doctors are seeing less instances of general illness. “Flu cases, in particular, are much lower than they have been in recent years at this point in the season, in part due to our efforts around social distancing, mask wearing, frequent hand washing and avoiding large gatherings,” says Dr. Holly Phillips, Board Certified General Internist. The moral of the story? Keep wearing a mask whenever you’re in public. Finding one that’s both comfortable and cute can help motivate you to avoid leaving home without one. Check out the medical grade disposable face masks in chic patterns like tie-dye and floral print by Barriere.

Of course, hand hygiene is key. “Soap and water is best, but hand sanitizer is a handy alternative when soap and water isn’t available,” Dr. Phillips advises. When you’re on the go, try a hand sanitizer that’s made from at least 60% ethanol or 70% isopropanol. (A great option: Life To Go’s Hand Sanitizer with Aloe Vera.)

And apply it generously! With hand sanitizer, “it should be enough to cover your palms, fingers and the bottom of your wrists,” cautions Dr. Phillips. Her quick tip for best results: “I recommend focusing on the tips of fingers in particular, as they’re very likely to come into contact with germs — think credit card keypads, elevator buttons, doorknobs, etc.”

Stay Healthy and Pretty Through Cold and Flu Season
Shutterstock

When using lots of hand sanitizer, “don’t forget to follow up with a good, toxin-free hand moisturizer,” says wellness expert Naomi Whittel. A great formula to try: Necessaire’s Hand Cream.

But maintaining good health isn’t just on the surface. “Getting enough nutrients is critical to maintaining a healthy immune system,” says Dr. Phillips. Give your diet a healthy boost with zinc, which can be found in chickpeas, yogurt and oysters, antioxidant Vitamin E found in nuts and green veggies like spinach and kale, Vitamin B6, plentiful in tuna, chicken and beans, and of course, Vitamin C, which Dr. Phillips says is a “critical immune system nutrient that needs to be replenished daily because the body doesn’t store it.” It’s found in citrus fruits, cantaloupe, strawberries and broccoli.

Another way to boost your nutrient intake is through supplements. Powdered vitamin mixes are a great option because they are mixed with water, which helps boost overall hydration. “Dehydration can put extra stress on the immune system, so staying hydrated also helps you stay healthy,” Dr. Phillips explains. A current favorite is Life To Go’s Immunity + Vitamin Drink Mix, containing zinc, Vitamin B6, Vitamin B12, a whopping 1,000 mg of Vitamin C plus 100 mg of elderberry. The gluten-free, vegan blend comes in the yummiest pink lemonade flavor!

For an immune-supportive diet, Whittel recommends including bone broth, collagen protein, MCT oil and fermented foods like sauerkraut or kimchee often.

Now just in case you’ve taken every measure to prevent getting sick but you happen to catch a cold, you can hide the effects in seconds! Conceal redness around the nose and mouth and your eyes with a concealer stick. Jones Road Beauty just launched The Face Pencil in 25 shades and the creamy formula glides on, blends seamlessly and stays put!

Given the constantly evolving nature of COVID-19, Us Weekly wants our readers to have access to the most accurate resources. For the most up-to-date coronavirus information, guidance, and support, consult the CDCWHO, and information from local public health officials. If you’re experiencing coronavirus symptoms, call your primary care provider for medical advice.

 

Flu shot side effects: What are they?

Flu shot side effects: What are they?

  • January 29, 2021

Some people who receive the flu shot may experience side effects. Often, these side effects are minor and temporary. Healthcare professionals recommend that those eligible for the flu vaccine get it annually.

The common side effects of the flu shot are much less severe than the symptoms of the flu and are unlikely to cause complications. However, in rare cases, people may experience serious side effects or allergic reactions to the flu shot.

This article will explain both the minor and serious side effects of the flu shot and how it works.

Some people may experience side effects after receiving the flu vaccine. These may differ from person to person and depending on the form of the vaccine.

Injectable flu shot

The side effects that most commonly occur with the injectable flu shot are local soreness, discoloration, and swelling at the injection site. Other possible side effects of the flu shot include:

Although it is uncommon, some people, especially children, may develop a low grade fever after vaccination, which is a response of the immune system. The cells of the immune system, which include lymphocytes and leukocytes, function better at a slightly higher body temperature.

The presence of a low grade fever after receiving a vaccination is a sign that the immune system is working. Anyone experiencing this symptom can treat it with over-the-counter medication.

Sometimes, people may faint after receiving an injection, including the flu shot. However, this is uncommon, and it is typically a reaction to the injection process rather than the flu shot specifically.

While not all experts agree, some evidence points to a small association between the flu shot and Guillain-Barré syndrome. Guillain-Barré syndrome occurs when the immune system attacks the nervous system. It is a rare condition but occurs more frequently in people who have had the flu shot.

Experts calculated the risk of developing Guillain-Barré syndrome after getting the flu shot. They estimated that the condition affects 1–2 people in every million who get the flu shot.

People should note that this complication is very rare and that the association is not well-documented.

Nasal flu vaccine

The nasal flu vaccine contains a live, attenuated virus that may cause some mild symptoms without leading to the flu. The side effects may include:

  • a runny nose
  • wheezing
  • headaches
  • vomiting
  • muscle aches
  • fever
  • a sore throat
  • a cough

Experts suggest that these side effects occur because the nasal vaccine contains live, weakened flu virus, as opposed to the inactivated virus in the flu shot.

Researchers have not seen an association between Guillain-Barré syndrome and the nasal vaccine.

Safety

Although people may experience side effects after receiving the flu shot or nasal vaccine, the side effects are less severe than the symptoms of the flu. Complications, hospitalization, and death can result from a flu infection, even in otherwise healthy people.

Conversely, flu vaccines are safe for most people. Over the past 50 years, hundreds of millions of people in the United States have received the flu shot without serious effects or complications.

The objective of flu vaccination programs is to limit the spread of the flu and establish herd immunity to protect those who cannot receive the flu vaccine. To establish herd immunity, a high percentage of people would need to get the vaccine, but this does not occur.

In the U.S., people may receive either a trivalent, inactivated influenza virus (TIV) vaccine or a live, attenuated, cold-adapted influenza virus (LAIV) vaccine. The TIV vaccine contains components of the killed virus, whereas the LAIV vaccine contains living, weakened virus.

Neither the TIV vaccine nor the LAIV vaccine causes the flu, but they both stimulate the immune system to provide protection against this illness.

Vaccination is an effective measure for preventing the flu and limiting its spread. People may also develop immunity by getting sick with the flu. However, as the flu can be serious, vaccination is the preferred route to immunity.

The two types of flu viruses that contribute to the annual flu epidemic are influenza A and influenza B.

You can learn more about these two types of influenza here.

Proteins called surface hemagglutinin surround the flu virus. These proteins attach to the cells in the human body and allow the virus to infect the person.

People develop immunity to the flu virus when the body creates antibodies against the surface hemagglutinin protein. When a person has exposure to the virus, antibodies against the surface hemagglutinin protect them by stopping the virus from attaching to the cells in the lungs and causing infection.

Vaccine manufacturers develop immunizations with this concept in mind. By exposing people to the killed or weakened viruses, the immune system can produce antibodies against the surface hemagglutinins.

Every year, people should contact a doctor or pharmacist to check whether they can receive the flu shot. The Centers for Disease Control and Prevention (CDC) recommend that anyone aged 6 months and above receive the annual flu vaccine.

However, some people should not get the flu shot, including those:

  • under 6 months of age
  • at known risk of life threatening allergic reactions to flu vaccines or ingredients in the vaccine
  • with severe egg allergies
  • with a history of Guillain-Barré syndrome

Doctors and other healthcare professionals can help people determine whether the flu shot is safe for them.

In rare cases, people may experience concerning side effects after receiving the flu shot, and they might require medical attention. Side effects that may be a cause for concern include:

  • high fever
  • behavioral changes
  • signs and symptoms of a severe allergic reaction

Severe allergic reactions are also rare, but people should look out for:

  • difficulty breathing
  • hoarseness or wheezing
  • swelling around the eyes or lips
  • hives
  • paleness
  • weakness
  • rapid heartbeat

These effects typically occur within minutes or hours of receiving the vaccine. Anyone experiencing these severe side effects should seek emergency medical attention.

Some people may experience mild side effects after receiving the flu shot. However, these side effects are significantly less severe than the symptoms of the flu. Even otherwise healthy people are at risk of complications, hospitalization, and death if they catch the seasonal flu.

In rare situations, people may experience severe side effects or allergic reactions. These effects typically occur immediately after vaccination, and doctors can manage them with medication. Anyone who has a severe reaction to a flu vaccine will not be eligible to receive another one in the future.

The more vaccinated people in the population, the less the virus spreads from person to person. Herd immunity protects people who cannot receive the flu shot.

The CDC recommend that people who can get the flu shot get vaccinated yearly.

Lake County News,California - A universal influenza vaccine may be one step closer, bringing long-lasting protection against flu

Lake County News,California – A universal influenza vaccine may be one step closer, bringing long-lasting protection against flu

  • January 29, 2021
Wouldn’t it be nice if one shot could protect you for life? Bryan R. Smith/AFP via Getty Images

A bad year for flu can mean tens of thousands of deaths in the U.S. Getting vaccinated can protect you from influenza, but you have to get the shot every year to catch up with the changing virus and to top up the short-lived immunity the vaccine provides. The vaccine’s effectiveness also depends on correct predictions about which strains will be most common in a given season.

For these reasons, a one-and-done universal vaccine that would provide lasting immunity over multiple flu seasons and protect against a variety of strains has been a long-term goal for scientists.

Researchers are now one step closer to hitting that target. Scientists recently completed the first human trial of a vaccine created by recombinant genetic technology to fool the immune system into attacking a part of the virus that does not change so fast and is common among different strains.

I am a microbiologist interested in infectious diseases, and I’ve followed the seasonal flu epidemic for several years. I’m excited by this news, which could mark the turning point in the quest for a universal flu vaccine. Here’s how it all works.

cross section of influenza virus showing RNA and surface proteins
3D model of an influenza virus. Its genetic material is inside, with proteins – HA in blue, NA in red – poking out from the surface. Smith Collection/GadoArchive Photos via Getty Images

Biology of the invading influenza virus

Like the virus that causes COVID-19, the influenza virus has a protein shell that is coated by a lipid membrane. Sticking through the membrane are multiple copies of three types of proteins: haemagglutinin, abbreviated as HA; neuraminidase, abbreviated as NA; and the matrix protein, M2.

It’s the properties of the HA and NA proteins that distinguish the different strains of the virus. You’ve probably heard of strains like H1N1 and H3N2, both of which are infecting people in the U.S. this year.

The HA molecule is shaped a bit like a flower bud, with a stalk and a head. Once someone inhales the virus, the tip of the HA molecule’s head binds to a receptor on the surface of the cells that line the person’s respiratory passages.

This initial binding is crucial as it induces the cell to engulf the virus. Once inside, the virus gets to work replicating its own genetic material. But the enzyme that copies its single-strand RNA is very sloppy; it can leave two or three mistakes, called mutations, in every new copy.

Sometimes the genetic changes are so drastic that the progeny viruses don’t survive; other times they are the start of new flu strains. Based on viral samples collected from around the world, the flu virus that arrives one year will have about seven new mutations in the gene for HA and four in the gene for NA compared to the previous year’s virus. These differences are a big part of why the same influenza vaccine won’t be as effective from one year to the next.

Immune cells fighting off flu with antibodies
Computer illustration of an immune cell (left) releasing many antibodies (white) to attack and disable invading flu particles. Juan Gaertner/Science Photo Library via Getty Images

Fighting off a flu infection

When infected with the flu virus, your immune system produces antibodies to fend it off. Most of these antibodies interact with the HA head and prevent the virus from getting into your cells.

But there’s a downside to that strong reaction. Because the immune response to the virus’s head is so vigorous, it pays little attention to other parts of the virus. That means that your immune system is not prepared to fend off any future infection with a virus that has a different HA head, even if the rest of the virus is identical.

Current flu vaccines are inactivated versions of the influenza virus and so also work by inducing antibodies targeted to the HA head. And that’s why each version of the vaccine usually works only against a particular strain. But, as the flu spreads, the rapid rate of genetic change can produce new versions of the HA head that will evade the antibodies induced by the vaccine. These newly resistant viruses will then render even the current season’s vaccine ineffective.

The stalk portion of the HA molecule is much more genetically stable than the head. And HA stalks from different flu strains are much more alike than their head regions are.

So, an obvious way to protect people against different flu strains would be to use just the HA stalk in a vaccine. Unfortunately vaccination with only a headless stalk doesn’t seem to prevent infection.

Scientists are currently pursuing several different solutions to this problem.

A new kind of flu vaccine

A team of scientists led by Florian Krammer at the Icahn School of Medicine at Mount Sinai just completed the first human clinical trial of what they hope will be a universal flu vaccine.

The researchers used recombinant genetic technology to create flu viruses with “chimeric” HA proteins – essentially a patchwork quilt built from pieces of different flu strains.

Volunteers for the clinical trial received two vaccinations separated by three months. The first dose consisted of an inactivated H1N1 virus with its original HA stalk but the head portion from a bird influenza virus. Vaccination with this virus induced a mild antibody response to the foreign head, and a robust response to the stalk. This pattern meant that the immune systems of the subjects had never encountered the head before, but had seen the stalk from previous flu vaccinations or infections.

The second vaccination consisted of the same H1N1 virus but with an HA head from a different bird virus. This dose elicited, again, a mild antibody response to the new head, but a further boost in response to the HA stalk. After each vaccine dose the subjects’ stalk antibody concentrations averaged about eight times higher than their initial levels.

Researchers found that even though the vaccine was based on the HA stalk of the H1N1 virus strain, the antibodies it elicited reacted to HA stalks from other strains too. In lab tests, the antibodies from vaccinated volunteers attacked the H2N2 virus that caused the 1957 Asian flu pandemic and the H9N2 virus that the CDC considers to be of concern for future outbreaks. The antibodies did not react to the stalk of the more distantly related H3 viral strain.

The antibody response also lasted a long time; after a year and a half, the volunteers still had about four times the concentration of antibodies to the HA stalk in their blood as when the trial started.

surface of influenza virus with HA proteins sticking out
Avoiding the vigorous immune response to the protein’s head means the immune cells can concentrate on the more stable stalk of the protein. Kateryna Kon/Science Photo Library via Getty Images

Since this was a phase 1 clinical trial testing only for adverse effects (which were minimal), the researchers didn’t expose vaccinated people to the flu to test if their new antibodies protected them.

However, they did inject the subjects’ blood serum, which contains the antibodies, into mice to see if it would protect them against the flu virus. Getting a shot of serum taken from volunteers a month after receiving the booster shot, when antibody levels were high, led to mice being 95% healthier after virus exposure than mice who got blood serum from nonvaccinated volunteers. Even the mice who received serum that was collected from vaccinated volunteers a year after the start of the trial were about 30% less sick.

These results show that vaccination with a chimeric flu protein can provide long-lasting immunity to several different strains of the influenza virus. Scientists will need to continue optimizing this approach so it works for different types and strains of influenza. But the success of this first human trial means you may one day get a single shot and, at last, be free from the flu.

[The Conversation’s science, health and technology editors pick their favorite stories. Weekly on Wednesdays.]The Conversation

Patricia L. Foster, Professor Emerita of Biology, Indiana University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

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