Is the Common Cold an Immune Overreaction?

Is the Common Cold an Immune Overreaction?

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It's my understanding that the majority of symptoms associated with the common cold (runny nose, inflamed sinus, slight fever) are essentially the result of the immune system's response.

I've never heard of someone dying of the common cold (unlike influenza), even in immune compromised people. As such, what damage would the cold virus inflict if there was no immune response? Would it be catastrophic?

Can someone die of the common cold?

No. The common cold is a clinical syndrome restricted to upper respiratory tract involvement. By clinical syndrome, I mean it is the constellation of symptoms (rather than the consequence of a specific pathogen). As you mention, these symptoms are the result of the immune response, rather than tissue damage or compromised function as a direct effect of a pathogen or its toxin (e.g., the watery diarrhea in cholera).

As defined (see, e.g., Cecil Medicine Ch. 369), this clinical syndrome cannot lead to death.

The common cold is an upper respiratory syndrome of rhinorrhea and nasal obstruction, frequently accompanied by sore throat, sneezing, and cough.

Can the viruses that cause the common cold cause death?

Yes. Many viruses that cause the common cold also cause other clinical syndromes that can cause death. This occurs when viral replication moves to the lower respiratory tract. As an example, influenza viruses are responsible for 25 - 30% of common colds (see Bennett, Principles and Practice of Infectious Disease, Ch.58). When it moves beyond the upper respiratory tract, influenza is responsible for substantial mortality. Other virus families that are responsible for both a common cold syndrome and lower respiratory tract syndrome in immunocompetent individuals (e.g., bronchiolitis, pneumonia) include parainfluenza virus, metapneumovirus, adenovirus, and (rarely) coronavirus. Rhinovirus, responsible for 40-50% of common cold cases, is uniquely unsuited to lower respiratory tract involvement, because of its preference for the cooler environment of the nasal mucosa, replicating best at 33 C (Murray Medical Microbiology, Ch 56). However, in individuals with Severe Combined Immunodeficiency (SCID), lower respiratory tract involvement does occur. There are a number of case series reporting death due to lower respiratory rhinovirus. This is an example.

Can the common cold lead to serious illnesses other than lower respiratory tract involvement?

Yes. Other morbidity can occur as a result of the immune response that produces the common cold syndrome. Rhinorrhea and congestion can progress to a viral rhinosinusitis, a separate syndrome with its own complications, or a secondary bacterial infection, which can lead to bacterial sinus involvement and/or bacterial lower respiratory tract infection. Otitis media is another common complication, especially in children, and has its own potential complications. Asthma (and, generally speaking, most lung diseases) can also be exacerbated by what would otherwise be a simple common cold and predisposes to lower respiratory tract involvement. Asthma does deserve special mention, because rhinovirus associated exacerbations can be fatal, but this is a consequence of asthma rather than a common cold syndrome. Further discussion of these syndromes are beyond the scope of the question, but are discussed briefly in the chapters referenced above.

The common cold is not the result of a single virus. Over 200 viruses can cause a cold, so specific symptoms could vary depending on the virus in question. However, in the absence of an immune response, the virus is may destroy bodily tissues as it completes its life cycle of infecting a cell, using the host cell machinery to replicate its genome, and causing the cell burst open and release the next generation of viruses. This destructive effect could lead to catastrophic symptoms. Especially since the infection is in your respiratory tract, severe tissue destruction could be fatal. It should be noted, though, that the infection generally subsides in a week even with a compromised adaptive immune system (like in HIV/AIDS). This is probably why you've never heard of people dying from the common cold, since it is likely that if their immune system is that compromised as to make such a thing possible, the cold would be the least of their problems.


The most common virus that causes the cold is the rhinovirus, which undergoes the lytic cycle:

clarification: as kindly pointed out by De Novo (thank you!), Rhinovirus itself does not lead to tissue destruction in respiratory epithelia. The Rhinovirus was mentioned simply as an example of the lytic cycle of viral replication, which results in the destruction (lysis) of infected cells and could result in tissue destruction.

In men, high testosterone can mean weakened immune response, study finds

Scientists at the Stanford University School of Medicine have linked high testosterone levels in men to a poor immune response to an influenza vaccine.

In a study published online Dec. 23 in the Proceedings of the National Academy of Sciences, the investigators show that men with relatively high amounts of circulating testosterone benefit less, as measured by a boost in protective antibodies after vaccination against influenza, than do men with lower testosterone levels and women.

In the study, women had a generally stronger antibody response to the vaccine than men. But the average response mounted by men with relatively low testosterone levels was more or less equivalent to that of women.

It has long been known that, for reasons that are not clear, men are more susceptible to bacterial, viral, fungal and parasitic infection than women are, and that men’s immune systems don’t respond as strongly as women’s to vaccinations against influenza, yellow fever, measles, hepatitis and many other diseases. The new study may explain why this is the case.

Women are known to have, on average, higher blood levels of signaling proteins that immune cells pass back and forth to jump-start inflammation, a key component of immune-system activation. Furthermore, previous research in animals and in cell-culture experiments has established that testosterone has anti-inflammatory properties, suggesting a possible interaction between the male sex hormone and immune response.

However, the new study found no connection between circulating levels of pro-inflammatory proteins and responsiveness to the flu vaccine. Nor does testosterone appear to directly chill immune response rather, it seems to interact with a set of genes in a way that damps that response, said the study’s senior author, Mark Davis, PhD, professor of microbiology and immunology and director of Stanford’s Institute for Immunity, Transplantation and Infection

“This is the first study to show an explicit correlation between testosterone levels, gene expression and immune responsiveness in humans,” said Davis, who is also the Burt and Marion Avery Family Professor of Immunology and a Howard Hughes Medical Institute investigator. “It could be food for thought to all the testosterone-supplement takers out there.”

The scientists took advantage of ongoing longitudinal research at Stanford. Since 2008, the research participants, who span a broad range of ages, have been getting blood drawn before and after receiving annual influenza vaccines. Many have returned year after year for their annual flu shots and associated blood draws. The participants’ samples are analyzed at Stanford’s Human Immune Monitoring Core, a distributed center deploying state-of-the-art instrumentation and expertise, for tens of thousands of variables, including circulating levels of numerous immune-signaling proteins counts of various blood-cell subtypes and the degree to which each of the roughly 22,000 genes in a participant’s circulating immune cells is active or inactive.

Sex differences

“Most studies don’t report on sex differences, a major determinant of variation in immune response,” said the study’s lead author, David Furman, PhD, a research associate in Davis’ group. The Stanford team, in collaboration with researchers at the French governmental research organization INSERM, aimed at probing those differences.

Analysis of samples from 53 women and 34 men showed that, on average, women had significantly stronger antibody responses to the influenza vaccine, consistent with other studies. “This was not surprising,” Furman said. The women also showed higher average pre-vaccination blood levels of pro-inflammatory immune-signaling proteins, as earlier studies have found. But pre-vaccination levels of those proteins in a particular woman’s blood didn’t significantly predict the degree of her post-vaccination antibody response.

The analysis also showed that, in men, elevated activity of a particular set of genes that tend to turn on and off at the same time was associated with a weakened antibody response to the vaccine. The same gene cluster’s activity levels didn’t track closely with antibody response in women.

This piqued the interest of Furman. Previous studies have shown that some of the constituent genes of this multi-gene cluster (known as Module 52) are involved in immune regulation — and that activation of the module is somehow boosted by testosterone.

So he, Davis and their colleagues looked directly at testosterone levels in their male subjects. They separated the 34 men into two groups — those whose circulating levels of testosterone in its bioactive form were above the median level, and those with below-median levels of the hormone. They found that, in the high-testosterone men, high-activation levels of Module 52 genes correlated with reduced post-vaccination antibody levels. In the low-testosterone men — as in women — activation levels of Module 52 genes bore no significant relationship to the amount of antibodies produced as a result of the influenza vaccine.

Testosterone effects

Additional analyses showed that testosterone reduces levels of certain transcription factors (regulatory proteins) that ordinarily prevent Module 52 genes from “turning on.” In other words, higher testosterone levels result in more Module 52 expression. Several Module 52 genes have known immune-system connections activation of one of these genes, for example, results in the accelerated differentiation of cells whose job it is to suppress, rather than foster, immune response. These connections make the interactions of the genes with testosterone an intriguing target of further exploration by immunologists, physiologists and drug researchers, Davis said.

But perhaps more intriguing, to many, is this: Why would evolution have designed a hormone that on the one hand enhances classic male secondary sexual characteristics, such as muscle strength, beard growth and risk-taking propensity, and on the other hand wussifies men’s immune systems?

The evolutionary selection pressure for male characteristics ranging from peacocks’ plumage to deer’s antlers to fighter pilots’ heroism is pretty obvious: Females, especially at mating-cycle peaks, prefer males with prodigious testosterone-driven traits.

Davis speculates that high testosterone may provide another, less obvious evolutionary advantage. “Ask yourself which sex is more likely to clash violently with, and do grievous bodily harm to, others of their own sex,” he said. Men are prone to suffer wounds from their competitive encounters, not to mention from their traditional roles in hunting, defending kin and hauling things around, increasing their infection risk.

While it’s good to have a decent immune response to pathogens, an overreaction to them — as occurs in highly virulent influenza strains, SARS, dengue and many other diseases — can be more damaging than the pathogen itself. Women, with their robust immune responses, are twice as susceptible as men to death from the systemic inflammatory overdrive called sepsis. So perhaps, Davis suggests, having a somewhat weakened (but not too weak) immune system can prove more lifesaving than life-threatening for a dominant male in the prime of life.

Other Stanford co-authors were Cornelia Dekker, MD, professor of pediatrics and medical director of the Stanford-LPCH Vaccine Program Robert Tibshirani, PhD, professor of statistics and of health research and policy and Noah Simon, PhD, a former postdoctoral scholar in Tibshirani’s group, now on the faculty of the University of Washington.

How do antibiotics help fight infections?

Antibiotics can be used to help your child's immune system fight infections by bacteria. However, antibiotics don’t work for infections caused by viruses. Antibiotics were developed to kill or disable specific bacteria. That means that an antibiotic that works for a skin infection may not work to cure diarrhea caused by bacteria. Using antibiotics for viral infections or using the wrong antibiotic to treat a bacterial infection can help bacteria become resistant to the antibiotic so it won't work as well in the future. It is important that antibiotics are taken as prescribed and for the right amount of time. If antibiotics are stopped early, the bacteria may develop a resistance to the antibiotics and the infection may come back again.

Note: Most colds and acute bronchitis infections will not respond to antibiotics. You can help decrease the spread of more aggressive bacteria by not asking your child’s healthcare provider for antibiotics in these cases.

In human cells and mice, a cure for the common cold, Stanford-UCSF study reports

Disabling a single, apparently noncritical protein in cells may foil replication of the viruses that cause half of all common colds, polio and other diseases, according to researchers at Stanford and UCSF.

Jan Carette is a senior author of a paper describing how he and his colleagues found a way to stop a broad range of enteroviruses, including rhinoviruses, from replicating inside human cells in culture, as well as in mice.
Paul Sakuma

Temporarily disabling a single protein inside our cells might be able to protect us from the common cold and other viral diseases, according to a study led by researchers at Stanford University and University of California-San Francisco.

The findings were made in human cell cultures and in mice.

“Our grandmas have always been asking us, ‘If you’re so smart, why haven’t you come up with a cure for the common cold?’”said Jan Carette, PhD, associate professor of microbiology and immunology. “Now we have a new way to do that.”

The approach of targeting proteins in our own cells also worked to stop viruses associated with asthma, encephalitis and polio.

Colds, or noninfluenza-related upper respiratory infections, are for the most part a weeklong nuisance. They’re also the world’s most common infectious illness, costing the U.S. economy an estimated $40 billion a year. At least half of all colds are the result of rhinovirus infections. There are roughly 160 known types of rhinovirus, which helps to explain why getting a cold doesn’t stop you from getting another one a month later. Making matters worse, rhinoviruses are highly mutation-prone and, as a result, quick to develop drug resistance, as well as to evade the immune surveillance brought about by previous exposure or a vaccine.

In a study published online Sept. 16 in Nature Microbiology, Carette and his associates found a way to stop a broad range of enteroviruses, including rhinoviruses, from replicating inside human cells in culture, as well as in mice. They accomplished this feat by disabling a protein in mammalian cells thatall enteroviruses appear to need in order to replicate.

Carette shares senior authorship with Or Gozani, MD, PhD, professor of biology at Stanford and the Dr. Morris Herzstein Professor of Biology Raul Andino, PhD, professor of microbiology and immunology at UCSF and Nevan Krogan, PhD, professor of cellular and molecular pharmacology at UCSF. The lead authors are former Stanford graduate student Jonathan Diep, PhD, and Stanford postdoctoral scholars Yaw Shin Ooi, PhD, and Alex Wilkinson, PhD.

Well-known and feared

One of the most well-known and feared enteroviruses is poliovirus. Until the advent of an effective vaccine in the 1950s, the virus spelled paralysis and death for many thousands of children each year in the United States alone. Since 2014, another type of enterovirus, EV-D68, has been implicated in puzzling biennialbursts of a poliolike disease, acute flaccid myelitis, in the United States and Europe. Other enteroviruses can cause encephalitis and myocarditis — inflammation of the brain and the heart, respectively.

Like all viruses, enteroviruses travel lightly. To replicate, they take advantage of proteins in the cells they infect.

To see what proteins in human cells are crucial to enteroviral fecundity, the investigators used a genomewide screen developed in Carette’s lab. They generated a cultured line of human cells that enteroviruses could infect. The researchers then used gene editing to randomly disable a single gene in each of the cells. The resulting culture contained, in the aggregate, cells lacking one or another of every gene in our genome.

The scientists infected the culture with RV-C15, a rhinovirus known to exacerbate asthma in children, and then with EV-C68, implicated in acute flaccid myelitis. In each case, some cells managed to survive infection and spawn colonies. The scientists were able to determine which gene in each surviving colony had been knocked out of commission. While both RV-C15 and EV-D68 are both enteroviruses, they’re taxonomically distinct and require different host-cell proteins to execute their replication strategies. So, most of the human genes encoding the proteins each viral type needed to thrive were different, too. But there were a handful of individual genes whose absence stifled both types’ ability to get inside cells, replicate, bust out of their cellular hotel rooms and invade new cells. One of these genes in particular stood out. This gene encodes an enzyme called SETD3. “It was clearly essential to viral success, but not much was known about it,” Carette said.

The scientists generated a culture of human cells lacking SETD3 and tried infecting them with several different kinds of enterovirus — EV-D68, poliovirus, three different types of rhinovirus and two varieties of coxsackievirus, which can cause myocarditis. None of these viruses could replicate in the SETD3-deficient cells, although all proved capable of pillaging cells whose SETD3-producing capability was restored.

The researchers observed a 1,000-fold reduction in a measure of viral replication inside human cells lacking SETD3, compared with controls. Knocking out SETD3 function in human bronchial epithelial cells infected with various rhinoviruses or with EV-D68 cut replication about 100-fold.

Impervious mice

Mice bioengineered to completely lack SETD3 grew to apparently healthy adulthood and were fertile, yet they were impervious to infection by two distinct enteroviruses that can cause paralytic and fatal encephalitis, even when these viruses were injected directly into the mice’s brains soon after they were born.

“In contrast to normal mice, the SETD3-deficient mice were completely unaffected by the virus,” Carette said. “It was the virus that was dead in the water, not the mouse.”

Enteroviruses,the scientists learned, have no use for the section of SETD3 that cells employ for routine enzymatic activity. Instead, enteroviruses cart around a protein whose interaction with a different part of the SETD3 molecule, in some as yet unknown way, is necessary for their replication.

“This gives us hope that we can develop a drug with broad antiviral activity against not only the common cold but maybe all enteroviruses, without even disturbing SETD3’s regular function in our cells,” Carette said.

Carette and Gozani are members of Stanford Bio-X and the Stanford Maternal & Child Health Research Institute, as well as faculty fellows of Stanford ChEM-H. Gozani is a member of the Stanford Cancer Institute.

Other Stanford co-authors are graduate student Christine Peters postdoctoral scholar James Zengel, PhD Siyuan Ding, PhD, instructor in medicine gastroenterology & hepatology basic life research scientist Kuo-Feng Weng, PhD former visiting research student Kristi Kobluk, DVM Joshua Elias, PhD, assistant professor of chemical and systems biology Peter Sarnow, PhD, professor of microbiology and immunology Harry Greenberg, MD, professor of gastroenterology and hepatology and of microbiology and immunology and Claude Nagamine, PhD, DVM, associate professor of comparative medicine.

Researchers at the Chan Zuckerberg Biohub and the VA Palo Alto Health Care System also contributed to the work.

Stanford’s departments of Microbiology and Immunology and of Biology also supported the work.

TikTok Users Convinced They Have Mystery Illness, Likely Just Common Cold

Users on TikTok have become captivated by an apparent new illness they're suffering, but the symptoms described appear similar to the common cold.

"Did anyone else get a little sick and thought it was allergies and they thought it was allergies and then it got worse. But it's not COVID, and it's not the flu, but they just can't figure out what it is, or is that just me?" said TikTok user @Sam22hunt, in a video shared one week ago. The clip has gained over one million likes at the time of publication.

"Did anyone start feeling bad, think it was allergies, but bam you have been sick for over a week and it's not COVID. And everyone I know that has it is a woman," wrote another user, with on-screen text in separate video.

"Same! I've had a cough/ runny nose for over a month," responded a viewer in the comments.

"Yes! I have mucus stuck in the back of my throat, a bad cough, not COVID tho," added another.

As reported by Vice, these mystery illness symptoms appear identical to those of a common cold.

Catherine Troisi, an infectious disease epidemiologist at UTHealth School of Public Health in Houston, told Vice's Motherboard: "When we talk about a cold there are actually hundreds of viruses that cause colds. That's why you keep getting them. That's why when you have a child in preschool, they are always bringing them home and you're catching them."

As most of us have been indoors for the past year, the spread of the common cold greatly lessened. Now social situations are entering our lives again, rates of the cold are increasing again. However, experts are unsure whether our immune systems have become more susceptible to the viruses in the meantime.

"It is true that we have not been exposed so much to colds during the last year. Whether our immune systems faded so much during that year to these viruses, we don't really know because we've never been in this situation before," Troisi told Motherboard.

"Theoretically it's possible that our immunity has waned somewhat, but I wouldn't say that's been proven and I wouldn't say that that's the only explanation," she added.

It's instead possible that a year's worth of COVID talk has simply caused TikTok users to forget about the common cold and its symptoms.

Elizabeth Scott, a microbiologist and associate dean and professor of Biology, College of Natural, Behavioral, and Health Sciences at Simmon's University, also told Motherboard that younger people, who happen to be TikTok's demographic, experience harsher symptoms.

"Generally speaking, children and young people experience more frequent colds and more severe symptoms, and TikTok users tend to be younger so the sample is biased in that respect," she said.

"The common cold is endemic in most human societies and it is not surprising that we are encountering it again as we start mingling more freely and without masks," she added. "I don't see it as a concern because whilst it is a misery to experience the cold symptoms, it is not a threat to our health."

Common Cold Coronaviruses Tied to Less Severe COVID-19 Cases

Anthony King
Nov 11, 2020

T here are four common cold coronaviruses that we all catch at some stage. We generate antibodies to them, but our immune memory of them fades over time, and we get re-infected.

Their names are all too easily forgotten—OC43, HKU1, 229E, and NL63—but our immune systems may nevertheless remember them for a time. There have been hints that exposure to these common coronaviruses might offer some protection from COVID-19, mostly by looking at signs of immune memory in blood samples taken from before the pandemic. A study in the Journal of Clinical Investigation reports the first clinical evidence linking recent endemic coronavirus infections to less severe COVID-19 and even a reduced death rate in patients.

“The COVID-19 disease is actually much less severe in those patients who had documented endemic coronavirus infections.”

The authors at Boston University School of Medicine found evidence for this by poring over the medical records of thousands of patients who had visited Boston Medical Center as inpatients or outpatients, most probably for respiratory illnesses, between 2015 and 2020. Each person had been assessed for infection using a PCR test that screens for bacteria and viruses, including the four endemic coronaviruses.

In total, 15,928 patients had at least one such PCR test. Of them, 875 tested positive for an endemic coronavirus (this group was called eCoV+), while the remaining 15,053 people never had a documented coronavirus infection (termed eCoV-).

Of the entire cohort, a total of 1,812 (11.4 percent) later returned for a SARS-CoV-2 test during the initial COVID-19 surge in Boston between March 12 and June 12.

“Our study is the first to examine people with known endemic coronavirus infections, and compare them to people who, as far as we know, don’t have any recent documented coronavirus infections,” says Manish Sagar, the lead author of the study and a virologist at Boston Medical Center.

The infection rate for SARS-CoV-2 was no different between those who had a recently recorded endemic coronavirus infection (eCoV+) and those who did not have a positive test (eCoV-). This led the authors to conclude that a recent infection with endemic coronaviruses did not keep SARS-CoV-2 at bay—both groups were just as likely to become infected with the pandemic virus.

When the researchers peered closer at the data, they observed an important difference between the two groups. “The COVID-19 disease is actually much less severe in those patients who had documented endemic coronavirus infections,” says Sagar. The odds of intensive care unit (ICU) admission were significantly lower in eCoV+ than in eCoV- patients, and there was “a trend towards lower odds of mechanical ventilation,” the authors write in their report.

The data also show that among hospitalized patients who had previous positive test results for endemic coronavirus, 4.8 percent of them died compared with 17.7 percent among those in the group without such a test result.

Local immune memory may help explain these results. Such “heterotypic immunity,” says immunologist Joseph Mizgerd, director of the pulmonary center at Boston University School of Medicine, occurs when immune memory is etched into the lungs and/or nose. It’s common after other types of respiratory infections and might offer protection against SARS-CoV-2 if elicited by endemic coronaviruses. Although the Boston group did not measure this type of immunity in patients, they now hypothesize that local immunity gained from endemic coronaviruses helps limit lung injury during COVID-19. “We are testing that in ongoing experiments,” Mizgerd says by email. He adds that such cross-reactive immunity is often mediated by memory T cells, which can localize in the lung, and he notes that lung-localized heterotypic T cells can prevent severe lung infection during pneumonias caused by other types of respiratory pathogens.

If indeed prior infection does ramp up protection against SARS-CoV-2, the study could not answer how long it takes for any such benefit to taper off. Nor did the work shed light on which of the four endemic coronaviruses in particular might be offering protection against the pandemic virus. The scientists are seeking funding to expand their research and include data from other institutions.

Mizgerd and his team did not look into which immune components may be responsible for an endemic coronavirus influencing a person’s immune response to SARS-CoV-2. This is something that immunologist Dennis Burton at the Scripps Research Institute in La Jolla, California, and his colleagues have investigated.

Since the start of the pandemic, they have been interested in whether pre-existing immune responses to seasonal coronaviruses could influence antibody responses to SARS-CoV-2. In a study published in September as a preprint on bioRxiv, Burton and colleagues compared serum antibodies and antibody-producing B cells from 36 donors sampled prior to the pandemic to see whether those antibodies reacted with the spike protein from the new pandemic virus. Very few antibodies from before the pandemic reacted to SARS-CoV-2, the team found. The vast majority did not bind strongly to the new virus, although they did identify one antibody that could neutralize SARS-CoV-2.

The group also detected memory B cells in blood samples from before the pandemic that were turned on by the presence of SARS-CoV-2. This activation triggered them to make antibodies that reacted against some proteins made by SARS-CoV-2. “That would suggest that there is some cross reactivity there,” says Burton.

“A cross-protective vaccine that protects against SARS-CoV-2 plus the endemic coronaviruses would be a really great boon.”

A recent Science study reported that 5 percent of 302 adults and 43 percent of 48 children had antibodies that reacted against certain proteins produced by SARS-CoV-2. Children are more prone to common cold coronavirus infections, perhaps explaining why they might harbor such antibodies, and why they suffer less severe COVID-19 symptoms.

“We do not know yet if the presence of such antibodies modifies the risk of becoming infected or the severity of disease,” senior author George Kassiotis at the Francis Crick Institute in London explains by email. There are conserved parts of the S2 peptide of the spike protein, such as the fusion peptide, in most coronaviruses “that are targeted by such cross-reactive and potentially cross-protective antibodies,” Kassiotis notes. This “may hold promise for a universal vaccine protecting against current, as well as future CoVs,” the authors write in their Science paper.

Kassiotis says that concerns that “antibody immunity might be short-lived have now been allayed” by recent studies and adds that even if antibodies fell below detectable levels, “the cells that made them will still be there and will respond faster and better to re-infection.”

Antibodies and B cells are part of only one aspect of our immune memory to viruses. Multiple investigations since the beginning of the pandemic have suggested that between 20 percent and 50 percent of people who had never encountered SARS-CoV-2 had T cells that nevertheless seemed to react against peptides from this virus, as noted recently in a Science paper.

In another study in Nature, researchers in Singapore identified memory T cells in patients who had recovered from SARS back in 2003. These were reactive to proteins from SARS-CoV-2, supporting the idea that T cell memory from infections with human coronaviruses may play a role in the response to an infection with the new pandemic virus.

An additional study recently published in Science used human blood samples from before the pandemic to locate parts of SARS-CoV-2 that stimulated existing T cells. The study found a range of memory T cells that could react to both the new virus and to the four common cold coronaviruses, again suggesting that existing T cells against common coronaviruses could play a role in the immune response to SARS-CoV-2 in some patients.

Immunologist Stanley Perlman of the University of Iowa who was not involved in any of these studies says that “everybody should have memory B cells against common cold coronaviruses.” We may also have memory T cells that remember these viruses and perhaps help with fighting SAR-CoV-2. However, Perlman emphasized that the implication of this for COVID-19 “is still a work in progress.”

Burton says he hopes to dig into a molecular understanding of the cross-reactivity of antibodies, which might help design a vaccine against not just SARS-CoV-2, but common cold coronaviruses too. These viruses usually cause mild symptoms, but not always.

“A cross-protective vaccine that protects against SARS-CoV-2 plus the endemic coronaviruses would be a really great boon,” says Sagar. “These coronaviruses are causes of the common cold, but they are also really important causes of pneumonia, pneumonia hospitalizations, and pneumonia deaths.”

Temperature-dependent innate defense against the common cold virus limits viral replication at warm temperature in mouse airway cells

Most isolates of human rhinovirus, the common cold virus, replicate more robustly at the cool temperatures found in the nasal cavity (33-35 °C) than at core body temperature (37 °C). To gain insight into the mechanism of temperature-dependent growth, we compared the transcriptional response of primary mouse airway epithelial cells infected with rhinovirus at 33 °C vs. 37 °C. Mouse airway cells infected with mouse-adapted rhinovirus 1B exhibited a striking enrichment in expression of antiviral defense response genes at 37 °C relative to 33 °C, which correlated with significantly higher expression levels of type I and type III IFN genes and IFN-stimulated genes (ISGs) at 37 °C. Temperature-dependent IFN induction in response to rhinovirus was dependent on the MAVS protein, a key signaling adaptor of the RIG-I-like receptors (RLRs). Stimulation of primary airway cells with the synthetic RLR ligand poly I:C led to greater IFN induction at 37 °C relative to 33 °C at early time points poststimulation and to a sustained increase in the induction of ISGs at 37 °C relative to 33 °C. Recombinant type I IFN also stimulated more robust induction of ISGs at 37 °C than at 33 °C. Genetic deficiency of MAVS or the type I IFN receptor in infected airway cells permitted higher levels of viral replication, particularly at 37 °C, and partially rescued the temperature-dependent growth phenotype. These findings demonstrate that in mouse airway cells, rhinovirus replicates preferentially at nasal cavity temperature due, in part, to a less efficient antiviral defense response of infected cells at cool temperature.

Keywords: RIG-I airway common cold innate immunity rhinovirus.

Conflict of interest statement

The authors declare no conflict of interest.


Temperature-dependent replication of rhinovirus and…

Temperature-dependent replication of rhinovirus and host response. ( A–D ) Cells were inoculated…

RLR signaling and activity in…

RLR signaling and activity in response to poly I:C is enhanced at 37…

IFN responsiveness is enhanced at…

IFN responsiveness is enhanced at 37 °C compared with 33 °C. ( A–F…

Replication of RV-1BM at 37…

Replication of RV-1BM at 37 °C is partially restored in airway cells deficient…


Asthma is another disease that involves increased levels of mucus in the airways. The airways are hypersensitive to particles like pollen or dust and when exposed, they become inflamed and produce excess mucus. The muscles around the airways tighten which narrows the space and breathing becomes difficult.

Coughing during an attack may also bring up sputum from the lungs, which is hard to expel.

Asthma attacks are usually treated with drugs that open the airways (bronchodilators) and by reducing exposure to allergens and conditions that bring it on.

How to prevent the common cold and flu

While immune support is essential year-round, it becomes critical during cold and flu season. Nutritional support can’t prevent us from becoming exposed to harmful viruses, but it can contribute to the body’s ability to protect itself as well as combat infections, as you’ll learn in Life Extension’s protocols for the common cold and influenza.

Science and Research About Maintaining Seasonal Support for a Healthy Immune System

Immune Seasonal Support Science & Research

Encourage the body’s healthy immune response to seasonal changes with vitamins, nutrients and plant compounds.

Frequently Asked Immune Seasonal Support Questions

Allergies represent an overreaction by the immune system. In a true allergy, the immune system responds to particles called antigens from normally harmless substances as if they were pathogenic invaders. The inflammatory response mounted by the immune system against an allergen can be serious, even life threatening. In cases where the immune system mounts a more conservative response to an allergen, a person may experience mild symptoms like headache, watery eyes and runny nose.

Allergies often have a genetic basis, so there is little that can be done to mitigate the allergic tendency. However, in milder cases, immunotherapy or exposure therapy under the supervision of a qualified healthcare provider may ameliorate an overzealous immune system. Immunotherapy should not be attempted without qualified supervision. In general, eating a healthy diet, exercising and maintaining a healthy weight—all of which discourage an inflammatory state in the body—may reduce the tendency toward inflammatory immune-mediated reactions. However, evidence is far from conclusive. Some preliminary studies suggest vitamin D supplementation may reduce symptoms of certain types of mild allergies, but the overall evidence is inconclusive.

Aging is associated with declining and potentially aberrant immune system function. This is known as immune senescence. Aging people may experience diminished efficacy of vaccines and a propensity toward immune-mediated inflammatory conditions, which may include some types of allergies. There is no conclusive evidence to suggest aging is associated with any particular allergy, but autoimmune diseases, systemic inflammation and allergic conditions in general may arise in the context of immune senescence. Some allergies, like atopic dermatitis and anaphylactic reactions to food allergens, appear to be less common with advancing age. However, one concern for aging people is drug allergy, which may be more of a concern in the context of multiple drugs (polypharmacy)—a common issue amongst older people.

White blood cells only make up a small percentage of your blood

The immune system is constantly at work to protect you from diseases and fight infections you already have, so you might expect that the system's soldiers — the white blood cells — would make up a large portion of your blood.

But this is not the case. White blood cells account for only 1 percent of the cells in the 5 liters of blood in an adult's body.

But don't worry, there are more than enough white blood cells to get the job done: In each microliter of blood, you have between 5,000 and 10,000 white blood cells.