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Study Finds People Have Short-Lived Immunity to Seasonal Coronaviruses

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Microscopic view of Coronavirus
Caption: Artistic rendering of coronaviruses. Credit: iStock/Naeblys

A key metric in seeking to end the COVID-19 pandemic is the likely duration of acquired immunity, which is how long people infected with SARS-CoV-2, the novel coronavirus that causes COVID-19, are protected against reinfection. The hope is that acquired immunity from natural infection—or from vaccines—will be long-lasting, but data to confirm that’s indeed the case won’t be in for many months or years.

In the meantime, a useful place to look for clues is in long-term data on reinfections with other seasonal coronaviruses. Could the behavior of less life-threatening members of the coronavirus family give us some insight into what to expect from SARS-CoV-2?

A new study, published in the journal Nature Medicine, has taken exactly this approach. The researchers examined blood samples collected continuously from 10 healthy individuals since the 1980s for evidence of infections—and reinfections—with four common coronaviruses. Unfortunately, it’s not particularly encouraging news. The new data show that immunity to other coronaviruses tends to be short-lived, with reinfections happening quite often about 12 months later and, in some cases, even sooner.

Prior to the discovery of SARS-CoV-2, six coronaviruses were known to infect humans. Four are responsible for relatively benign respiratory illnesses that regularly circulate to cause the condition we recognize as the common cold. The other two are more dangerous and, fortunately, less common: SARS-CoV-1, the virus responsible for outbreaks of Severe Acute Respiratory Syndrome (SARS), which ended in 2004; and MERS-CoV, the virus that causes the now rare Middle East Respiratory Syndrome (MERS).

In the new study, a team led by Lia van der Hoek, University of Amsterdam, the Netherlands, set out to get a handle on reinfections with the four common coronaviruses: HCoV-NL63, HCoV-229E, HCoV-OC43, and HCoV-HKU1. This task isn’t as straightforward as it might sound. That’s because, like SARS-CoV-2, infections with such viruses don’t always produce symptoms that are easily tracked. So, the researchers looked instead to blood samples from 10 healthy individuals enrolled for decades in the Amsterdam Cohort Studies on HIV-1 Infection and AIDS.

To detect coronavirus reinfections, they measured increases in antibodies to a particular portion of the nucleocapsid of each coronavirus. The nucleocapsid is a protein shell that encapsulates a coronavirus’ genetic material and serves as important targets for antibodies. An increase in antibodies targeting the nucleocapsid indicated that a person was fighting a new infection with one of the four coronaviruses.

All told, the researchers examined a total of 513 blood samples collected at regular intervals—every 3 to 6 months. In those samples, the team’s analyses uncovered 3 to 17 coronavirus infections per study participant over more than 35 years. Reinfections occurred every 6 to 105 months. But reinfections happened most frequently about a year after a previous infection.

Not surprisingly, they also found that blood samples collected in the Netherlands during the summer months—June, July, August, and September—had the lowest rate of infections for all four seasonal coronaviruses, indicating a higher frequency of infections in winter in temperate countries. While it remains to be seen, it’s possible that SARS-CoV-2 ultimately may share the same seasonal pattern after the pandemic.

These findings show that annual reinfections are a common occurrence for all other common coronaviruses. That’s consistent with evidence that antibodies against SARS-CoV-2 decrease within two months of infection [2]. It also suggests that similar patterns of reinfection may emerge for SARS-CoV-2 in the coming months and years.

At least three caveats ought to be kept in mind when interpreting these data. First, the researchers tracked antibody levels but didn’t have access to information about actual illness. It’s possible that a rise in antibodies to a particular coronavirus might have provided exactly the response needed to convert a significant respiratory illness to a mild case of the sniffles or no illness at all.

Second, sustained immunity to viruses will always be disrupted if the virus is undergoing mutational changes and presenting a new set of antigens to the host; the degree to which that might have contributed to reinfections is not known. And, third, the role of cell-based immunity in fighting off coronavirus infections is likely to be significant, but wasn’t studied in this retrospective analysis.

To prepare for COVID-19 this winter, it’s essential to understand how likely a person who has recovered from the illness will be re-infected and potentially spread the virus to other people. While much more study is needed, the evidence suggests it will be prudent to proceed carefully and with caution when it comes to long-term immunity, whether achieved through naturally acquired infections or vaccination.

While we await a COVID-19 vaccine, the best way to protect yourself, your family, and your community is to take simple steps all of us can do today: maintain social distancing, wear a mask, avoid crowded indoor gatherings, and wash your hands.

References:

[1] Seasonal coronavirus protective immunity is short-lasting. Edridge AWD, Kaczorowska J, Hoste ACR, Bakker M, Klein M, Loens K, Jebbink MF, Matser A, Kinsella CM, Rueda P, Ieven M, Goossens H, Prins M, Sastre P, Deijs M, van der Hoek L. Nat Med. 2020 Sep 14. doi: 10.1038/s41591-020-1083-1. [Published online ahead of print.]

[2] Rapid decay of anti-SARS-CoV-2 antibodies in persons with mild Covid-19. Ibarrondo FJ, Fulcher JA, Goodman-Meza D, Elliott J, Hofmann C, Hausner MA, Ferbas KG, Tobin NH, Aldrovandi GM, Yang OO. N Engl J Med. 2020 Sep 10;383(11):1085-1087.

Links:

Coronavirus (COVID-19) (NIH)

Lia van der hoek (University of Amsterdam, the Netherlands)


Immune T Cells May Offer Lasting Protection Against COVID-19

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Healthy human T Cell
Caption: Scanning electron micrograph of a human T lymphocyte (T cell) from a healthy donor’s immune system. Credit: National Institute of Allergy and Infectious Diseases/NIH

Much of the study on the immune response to SARS-CoV-2, the novel coronavirus that causes COVID-19, has focused on the production of antibodies. But, in fact, immune cells known as memory T cells also play an important role in the ability of our immune systems to protect us against many viral infections, including—it now appears—COVID-19.

An intriguing new study of these memory T cells suggests they might protect some people newly infected with SARS-CoV-2 by remembering past encounters with other human coronaviruses. This might potentially explain why some people seem to fend off the virus and may be less susceptible to becoming severely ill with COVID-19.

The findings, reported in the journal Nature, come from the lab of Antonio Bertoletti at the Duke-NUS Medical School in Singapore [1]. Bertoletti is an expert in viral infections, particularly hepatitis B. But, like so many researchers around the world, his team has shifted their focus recently to help fight the COVID-19 pandemic.

Bertoletti’s team recognized that many factors could help to explain how a single virus can cause respiratory, circulatory, and other symptoms that vary widely in their nature and severity—as we’ve witnessed in this pandemic. One of those potential factors is prior immunity to other, closely related viruses.

SARS-CoV-2 belongs to a large family of coronaviruses, six of which were previously known to infect humans. Four of them are responsible for the common cold. The other two are more dangerous: SARS-CoV-1, the virus responsible for the outbreak of Severe Acute Respiratory Syndrome (SARS), which ended in 2004; and MERS-CoV, the virus that causes Middle East Respiratory Syndrome (MERS), first identified in Saudi Arabia in 2012.

All six previously known coronaviruses spark production of both antibodies and memory T cells. In addition, studies of immunity to SARS-CoV-1 have shown that T cells stick around for many years longer than acquired antibodies. So, Bertoletti’s team set out to gain a better understanding of T cell immunity against the novel coronavirus.

The researchers gathered blood samples from 36 people who’d recently recovered from mild to severe COVID-19. They focused their attention on T cells (including CD4 helper and CD8 cytotoxic, both of which can function as memory T cells). They identified T cells that respond to the SARS-CoV-2 nucleocapsid, which is a structural protein inside the virus. They also detected T cell responses to two non-structural proteins that SARS-CoV-2 needs to make additional copies of its genome and spread. The team found that all those recently recovered from COVID-19 produced T cells that recognize multiple parts of SARS-CoV-2.

Next, they looked at blood samples from 23 people who’d survived SARS. Their studies showed that those individuals still had lasting memory T cells today, 17 years after the outbreak. Those memory T cells, acquired in response to SARS-CoV-1, also recognized parts of SARS-CoV-2.

Finally, Bertoletti’s team looked for such T cells in blood samples from 37 healthy individuals with no history of either COVID-19 or SARS. To their surprise, more than half had T cells that recognize one or more of the SARS-CoV-2 proteins under study here. It’s still not clear if this acquired immunity stems from previous infection with coronaviruses that cause the common cold or perhaps from exposure to other as-yet unknown coronaviruses.

What’s clear from this study is our past experiences with coronavirus infections may have something important to tell us about COVID-19. Bertoletti’s team and others are pursuing this intriguing lead to see where it will lead—not only in explaining our varied responses to the virus, but also in designing new treatments and optimized vaccines.

Reference:

[1] SARS-CoV-2-specific T cell immunity in cases of COVID-19 and SARS, and uninfected controls. Le Bert N, Tan AT, Kunasegaran K, et al. Nature. 2020 July 15. [published online ahead of print]

Links:

Coronavirus (COVID-19) (NIH)

Overview of the Immune System (National Institute of Allergy and Infectious Diseases/NIAID)

Bertoletti Lab (Duke-NUS Medical School, Singapore)


Will Warm Weather Slow Spread of Novel Coronavirus?

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Summer gear and a face mask
Credit: Modified from iStock/energyy

With the start of summer coming soon, many are hopeful that the warmer weather will slow the spread of SARS-CoV-2, the novel coronavirus that causes COVID-19. There have been hints from lab experiments that increased temperature and humidity may reduce the viability of SARS-CoV-2. Meanwhile, other coronaviruses that cause less severe diseases, such as the common cold, do spread more slowly among people during the summer.

We’ll obviously have to wait a few months to get the data. But for now, many researchers have their doubts that the COVID-19 pandemic will enter a needed summertime lull. Among them are some experts on infectious disease transmission and climate modeling, who ran a series of sophisticated computer simulations of how the virus will likely spread over the coming months [1]. This research team found that humans’ current lack of immunity to SARS-CoV-2—not the weather—will likely be a primary factor driving the continued, rapid spread of the novel coronavirus this summer and into the fall.

These sobering predictions, published recently in the journal Science, come from studies led by Rachel Baker and Bryan Grenfell at Princeton Environmental Institute, Princeton, NJ. The Grenfell lab has long studied the dynamics of infectious illnesses, including seasonal influenza and respiratory syncytial virus (RSV). Last year, they published one of the first studies to look at how our warming climate might influence those dynamics in the coming years [2].

Those earlier studies focused on well-known human infectious diseases. Less clear is how seasonal variations in the weather might modulate the spread of a new virus that the vast majority of people and their immune systems have yet to encounter.

In the new study, the researchers developed a mathematical model to simulate how seasonal changes in temperature might influence the trajectory of COVID-19 in cities around the world. Of course, because the virus emerged on the scene only recently, we don’t know very much about how it will respond to warming conditions. So, the researchers ran three different scenarios based on what’s known about the role of climate in the spread of other viruses, including two coronaviruses, called OC43 and HKU1, that are known to cause common colds in people.

In all three scenarios, their models showed that climate only would become an important seasonal factor in controlling COVID-19 once a large proportion of people within a given community are immune or resistant to infection. In fact, the team found that, even if one assumes that SARS-CoV-2 is as sensitive to climate as other seasonal viruses, summer heat still would not be enough of a mitigator right now to slow its initial, rapid spread through the human population. That’s also clear from the rapid spread of COVID-19 that’s currently occurring in Brazil, Ecuador, and some other tropical nations.

Over the longer term, as more people develop immunity, the researchers suggest that COVID-19 may likely fall into a seasonal pattern similar to those seen with diseases caused by other coronaviruses. Long before then, NIH is working intensively with partners from all sectors to make sure that safe, effective treatments and vaccines will be available to help prevent the tragic, heavy loss of life that we’re seeing now.

Of course, climate is just one key factor to consider in evaluating the course of this disease. And, there is a glimmer of hope in one of the group’s models. The researchers incorporated the effects of control measures, such as physical distancing, with climate. It appears from this model that such measures, in combination with warm temperatures, actually might combine well to help slow the spread of this devastating virus. It’s a reminder that physical distancing will remain our best weapon into the summer to slow or prevent the spread of COVID-19. So, keep wearing those masks and staying 6 feet or more apart!

References:

[1] Susceptible supply limits the role of climate in the early SARS-CoV-2 pandemic. Baker RE, Yang W, Vecchi GA, Metcalf CJE, Grenfell BT. Science. 2020 May 18. [Online ahead of print.]

[2] Epidemic dynamics of respiratory syncytial virus in current and future climates. Baker RE, Mahmud AS, Wagner CE, Yang W, Pitzer VE, Viboud C, Vecchi GA, Metcalf CJE, Grenfell BT.Nat Commun. 2019 Dec 4;10(1):5512.

Links:

Coronavirus (COVID-19) (NIH)

Bryan Grenfell (Princeton University, Princeton, NJ)

Rachel Baker (Princeton University, Princeton, NJ)


Possible Explanation for Why Some People Get More Colds

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Cough

Getty Images/yourstockbank

Colds are just an occasional nuisance for many folks, but some individuals seem to come down with them much more frequently. Now, NIH-funded researchers have uncovered some new clues as to why.

In their study, the researchers found that the cells that line our airways are quite adept at defending against cold-causing rhinoviruses. But there’s a tradeoff. When these cells are busy defending against tissue damage due to cigarette smoke, pollen, pollutants, and/or other airborne irritants, their ability to fend off such viruses is significantly reduced [1].

The new findings may open the door to better strategies for preventing the common cold, as well as other types of respiratory tract infections caused by non-flu viruses. Even small improvements in prevention could have big implications for our nation’s health and economy. Every year, Americans come down with more than 500 million colds and similar infections, leading to reduced work productivity, medical expenses, and other costs approaching $40 billion [2].