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A naturopath reveals the cold and flu supplements that actually work

  • May 18, 2021

We speak with an expert in natural health and wellness about how to keep sickness at bay this winter. 

Winter is coming and Australians are once again facing a double threat of flu and COVID-19, so it’s more important than ever to make sure we have a strong immune system in place to ward off viruses.

Eating well, getting enough sleep, and maintaining a regular fitness routine are all crucial for immunity but there are also a few ways to supplement good health.

After almost 20 years in the health industry working as a naturopath, herbalist and naturopathy lecturer at the largest private higher education provider of natural health courses in the Southern Hemisphere – Endeavour College of Natural Health, I’ve come across some cold and flu remedies that have become staples during the cooler months to boost immunity and stay fighting fit.

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Andrographis

Andrographis (also known as Indian echinacea) has been shown to be acutely effective for colds and flus but it’s important to note that it should only be taken in short bursts. There were some stories during the pandemic about Andrographis supplements causing loss of taste and this highlighted the need to follow instructions and consult a professional to avoid side effects from overuse.

Recent research also showed that Andrographis (along with green tea, Vitamins C, D and zinc) lowered symptom severity and duration of respiratory events via immune modulation, inflammatory regulation and viral control. Andrographis may be protective for patients at risk of severe consequences from infection.

Elderberry

Elderberry isn’t as well-known as Vitamin C but it packs a punch when it comes to immunity and assisting with colds and flus. It’s one of most researched herbs and has been shown to be effective against viral infections. The little known berry skyrocketed to fame when Miranda Kerr touted its benefits during the pandemic.

Medicinal mushrooms

Medicinal mushrooms like Reishi, Shitake, Cordyceps and Coriolus may have beneficial effects on our immune response by enhancing immune function and providing antiviral and antibacterial actions. They can trigger the production of Natural Killer cells, which help us fight back against invading pathogens, which may help us recover from infections while providing resistance to illness.

In addition they are beneficial for our gut microbiome in many ways including acting as a prebiotic source which supplies food for our beneficial flora and also via signalling to our immune system. In addition, medicinal mushrooms are nourishing for our adrenal glands and can help us cope with stress. These mushrooms with benefits usually come in a powder form and can be mixed with plant based milks and honey.

Probiotics

Considering that 80 per cent of the immune system resides in the gut, this is a crucial area to support in winter and probiotics are a great tool for good gut health. These tiny live organisms, which we consume in the billions (of colony forming units), can have a big impact on our physical wellbeing.

Their antimicrobial effect in the gut promotes immune modulation which makes them an effective tool against allergic and inflammatory responses while at the same time improving resistance to pathogens.

Propolis

Propolis is always in my handbag in winter and whenever I travel, especially on planes. Produced as a by-product of honey production, bees use the sticky substance to coat the inside of the hive and it does the same thing in our throat, reducing the likelihood of bacteria taking hold or infecting the host, which may protect against catching a virus.

It’s also valued for its antimicrobial, antiviral and antifungal properties, which have been shown to be effective against viruses like influenza. It may also be useful for sore throats, ear infections and any mild upper respiratory tract infection.

Vitamin C

Long touted for its ability to reduce cold and flu symptoms and ramp up immunity, Vitamin C is one of the most popular supplements in the world. For the best impact against a cold or flu, try liposomal formulations of Vitamin C which have been shown to improve absorption – up to 93 per cent compared to 17 per cent for regular Vitamin C capsules.

Vitamin D

The sunshine vitamin really came into its own during the pandemic with a lot of studies showing how important it was in the fight against COVID-19. It has even been proposed that vitamin D supplementation could help reduce the severity of a flu for nursing home residents.

It has long been known that Vitamin D is useful when it comes to immunity but it’s estimated that 30-50 per cent of us could be deficient. A daily supplement can top up regular bursts of sunshine.

Zinc

Zinc is one of my favourite supplements, especially when it is in a readily available form like citrate or glycinate for better absorption. Zinc can help with many modern ailments including immunity, as long as it’s taken in the right dose – around 25-50mg daily.

Some research during the pandemic showed that absorption was markedly increased when taken with ECGC (from green tea) to increase zinc’s anti-viral activity while other studies revealed that COVID-19 patients lacking in zinc developed more complications.

Always seek the advice of a health practitioner and speak to your Naturopath before self-prescribing herbal medicine, especially if you are taking any other medication. Fin Mackenzie is a naturopath, Naturopathic & Nutritional Medicine Lecturer at Endeavour College of Natural Health, and founder of Green Door Health.

A COVID-19 vaccine in intranasal form in front of several out of focus vials of COVID-19 vaccine.

Nasal Vaccines for COVID-19? | MedPage Today

  • May 11, 2021

Despite an arsenal of highly effective injectable vaccines, drugmakers are looking into products that will be easier to store, transport, and administer in the global crisis — particularly, intranasal vaccines.

Could these vaccines also hold an advantage when it comes to blocking transmission? While more data has suggested the vaccines authorized in the U.S. cut transmission, some experts have argued that intranasal vaccines may do an even better job of this.

MedPage Today surveyed the global landscape of intranasal vaccines in development, the majority of which are in early stages.

Rationale for COVID-19 Mucosal Vaccines

The mucosal immune system represents the body’s first line of defense against outside pathogens at surfaces like the nose, lungs, mouth, eyes, and GI tract. Because the nasopharynx is the primary entry point for SARS-CoV-2, targeting the nasal cavity could be one of the best lines of defense for vaccines, according to Michael Russell, PhD, an emeritus professor of microbiology and immunology at the University at Buffalo in New York.

“By generating effective mucosal immune responses, it should be possible to forestall coronavirus infection from the outset, and also more effectively reduce transmission of the virus,” Russell told MedPage Today. “Nasal immunization aims to replicate this natural immunization process in a more effective manner.”

Current injectable vaccines induce a systemic immune response by generating circulating IgG antibodies that neutralize pathogens before they can cause severe tissue damage. But IgG is not very good at controlling viral entry into the body. To do that, the mucosal immune system is needed. It produces secretory IgA at the site of viral entry, and in larger quantities than any other type of immunoglobulin in the body.

“The major advantage of mucosal vaccines would be to create a strong immune response at the initial site of virus entry. If you can stop the virus here, it won’t be able to get into the lungs to cause damage,” said Richard Kennedy, PhD, who studies the development of immune responses after vaccination at the Mayo Clinic.

IgA also seems to be important in early infection. In one study, researchers measured immune responses in 159 patients with COVID-19. They found that IgA dominated the early stage of infection, peaked 3 weeks after symptom onset, and neutralized virus better than IgG. The results suggest that IgA-mediated mucosal immunity may decrease infectivity of the virus in human secretions and decrease viral transmission, according to the authors.

Mucosal Vaccines in the Pipeline

While mucosal vaccines may hold promise, clinical trials have only recently begun. Among 96 vaccine candidates in clinical trials, just eight are intranasal vaccines. Clinical trials are being conducted in the U.S., U.K., China, India, Cuba, and Iran, according to World Health Organization data released on May 5.

Two intranasal vaccine candidates are in phase II clinical trials. One uses a live-attenuated influenza virus adapted to express the spike protein of SARS-CoV-2, and is being developed by the University of Hong Kong, Xiamen University, and the Beijing Wantai Biological Pharmacy Enterprise, in partnership with the Coalition for Epidemic Preparedness Innovations (CEPI). The second is a protein subunit vaccine that is being developed by Razi Vaccine and Serum Research Institute in Iran.

In the U.S., two intranasal vaccine candidates are in phase I trials. The first is Altimmune’s nonreplicating adenoviral vector vaccine called AdCOVID. On March 25, the company released preclinical results in mice suggesting that the vaccine was protective against illness, decreased levels of replicating virus in the nose and respiratory tract, and produced a “robust” IgG response. Past results in mice had shown that IgA antibodies were maintained for at least 6 months after a single dose of the vaccine.

The second is Meissa’s live-attenuated candidate. Preclinical data in nonhuman primates have suggested that the candidate induced mucosal IgA and serum neutralizing antibodies, and was “highly protective” against infection with SARS-CoV-2 in the upper and lower respiratory tract.

Other intranasal vaccine candidates in clinical trials include: Cuba’s Center for Genetic Engineering & Biotech protein subunit vaccine (phase I/II); the University of Oxford/AstraZeneca’s Covishield, a nasal spray version of its ChadOx1 vaccine (phase I); Codagenix/Serum Institute of India’s live-attenuated SARS CoV-2 COVI-VAC vaccine (phase I); and India’s Bharat Biotech’s non-replicating adenoviral vector vaccine.

Recently, China’s CanSino Biologics announced plans to start a phase I/II trial of another inhaled vaccine, according to an emailed news release from the data and analytics company Global Data.

Because SARS-CoV-2 also infects the GI tract, another potential site of mucosal immunity, oral vaccines are also in clinical trials. Maryland’s Vaxart recently announced that it will be advancing one oral vaccine candidate to a phase II trial, and two oral vaccine candidates to phase I/II trials. California’s Immunity Bio has a nonreplicating human adenoviral vector vaccine in a phase Ib trial, and Symvivo/Merck’s DNA-based vaccine is in a phase I trial in Australia.

Advantages and Drawbacks

Both oral and intranasal vaccines offer the advantage of being stable at room temperature, making them easier to ship and potentially improving access to vaccination in remote or resource-poor settings. Both offer the advantage of easier administration, in the form of a nasal spray, pill, or drop on the tongue. That, in turn, may help improve acceptance, especially among children and the needle-shy, Russell said.

Nevertheless, mucosal vaccines do have drawbacks. While they can produce both systemic and local immunity, one stumbling block is producing effective, long-lasting immunity. Mucosal surfaces contain various barriers to pathogens — high acidity in the upper GI tract, sticky layers of mucous in the respiratory system — which may interfere with the ability of vaccines to access and activate the mucosal immune system. That could contribute to poor immunogenicity and faster waning immunity.

For instance, the intranasal flu vaccine FluMist has had a rocky road, in part because of lower effectiveness compared to injectable flu vaccines.

“There are not many licensed mucosal vaccines,” Kennedy said. “These vaccines are effective for certain pathogens, but this may or may not be true for SARS-CoV-2.”

Safety is another consideration. The majority of mucosal vaccines licensed in the U.S. are delivered via the oral route. Perhaps because of closer proximity to the brain, vaccine regulators appear to have shied away from the intranasal route. For example, Berna Biotech’s inactivated intranasal influenza vaccine was discontinued in Switzerland after it was found to be associated with increased risk of Bell’s Palsy.

Still, because oral vaccination tends to produce an antibody response that is not so strong in the respiratory tract, Russell contends that intranasal immunization “makes the most sense” for a respiratory pathogen like SARS-CoV-2.

“If similar resources can be made available for the accelerated development of intranasal vaccines, as have been deployed for the existing vaccines, my guess is that we might see some of them becoming available within about a year,” he said.

Infusion Improves Immune Response of Aging Frailty Following Flu Shot — Precision Vaccinations

Infusion Improves Immune Response of Aging Frailty Following Flu Shot — Precision Vaccinations

  • April 15, 2021
(Precision Vaccinations)

Florida-based Longeveron Inc. announced the completion of the Company’s Phase I/II clinical study of the use of Lomecel-B to improve immune response to influenza vaccine in subjects with Aging Frailty.

Longeveron stated in a press release issued on April 15, 2021, ‘it is anticipated that the top-line trial results will be announced in the 3rd quarter of 2021.’

Lomecel-B is an allogeneic, bone marrow-derived medicinal signaling cell product manufactured under current good manufacturing practices by Longeveron.  

The company says ‘Lomecel-B has the potential to reduce inflammation associated with Aging Frailty and to promote an anti-inflammatory state by releasing anti-inflammatory molecules, which can balance the immune system and improve the function of B lymphocytes.

As B cells are responsible for antibody production in response to vaccines, Lomecel-B may boost antibody generation and immunity following vaccination in subjects with Aging Frailty.’

“Completion of this clinical study to investigate Lomecel-B as a new therapeutic approach to boost immune response serves as an important initial step to meet the critical unmet medical need for those with Aging Frailty, who often respond poorly to vaccines,” said Sean Leng, MD, Ph.D., Professor of Medicine, Molecular Microbiology and Immunology at Johns Hopkins University School of Medicine and Bloomberg School of Public Health and the study’s principal investigator.

Aging Frailty is a life-threatening geriatric condition affecting approximately 15% of Americans over 65 or 8.1 million individuals. Aging Frailty patients are vulnerable to poor clinical outcomes compared to their age-matched peers despite sharing similar comorbidities and demographics. Therefore it is considered by some as an extreme form of unsuccessful aging. 

Geoff Green, CEO of Longeveron. “From the inception of Longeveron, we have focused our efforts on using a regenerative medicine approach to treat chronic, aging-related diseases and conditions, such as frailty and Alzheimer’s disease, with the goal of improving healthspan.”

Miami-based Longeveron is a clinical-stage biotechnology company developing cellular therapies for specific aging-related and life-threatening conditions.

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

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