#15,881
Viral interference - the ability of one circulating virus to inhibit or impede the transmission of another - while not completely understood, has been well documented and has been a frequent topic of conversation over the years in this blog (see When Epidemic Viruses Collide).
An early example, during the 2009 H1N1 pandemic some countries reported widespread rhinovirus outbreaks in the fall of 2009 while seeing far less H1N1 activity than expected (see 2009 New Scientist article Common cold may hold off swine flu).
And of course, over the past year, influenza, RSV, the common cold, and other respiratory viruses have practically fallen off a cliff between the use of facemasks, social distancing, and (potentially) viral interference caused by COVID-19.
While the exact mechanism behind this subduing of competing viruses is an ongoing topic of research, many researchers believe that exposure to one virus activates not only a targeted immune response - but also the body's innate immune response - essentially raising `shields' against other possible viral invaders.
A heightened immune response that may persist of weeks or even months, an idea that has been dubbed the `temporary immunity hypothesis'.
In 2017's PLoS Comp. Bio.: Spring & Early Summer Most Likely Time For A Pandemic, researchers used `viral interference' and/or the temporary immunity hypothesis to explain why historically pandemics almost always emerge in the spring or early summer; after the end of regular flu season.
The current interaction between COVID-19 and other respiratory viruses - which have been greatly subdued for a full year - raises a lot of questions about what happens when COVID eventually recedes, and these other viruses come back to the fore (see COVID-19, The Next Flu Season, And The Temporary Immunity Hypothesis).
While it may not answer those questions, we've a new study today out of the University of Glasgow that finds at least one common Rhinovirus (A16) inhibits infection of (in vitro) human respiratory epithelium cells by the SARS-CoV-2 virus.
This protective effect is far from absolute, of course. And its impact in the lab may not translate well to its impact in the field. Also, this study only looks at the impact of one (of hundreds) of common respiratory viruses.
Nevertheless, understanding the interaction between circulating viruses - particularly during and immediately following a pandemic - may be crucial if we are to successfully anticipate and prepare for what comes next with COVID-19, and pandemics and epidemics that will follow.
First, a link and the abstract from the open-access study, followed by excerpts from a press release by the University of Glasgow, and finally some expert reactions from the Science Media Centre.
Human rhinovirus infection blocks SARS-CoV-2 replication within the respiratory epithelium: implications for COVID-19 epidemiology
Dee, K., Goldfarb, D. M., Haney, J., Amat, J. A.R., Herder, V., Stewart, M., Szemiel, A. M., Baguelin, M. and Murcia, P. R. (2021) Human rhinovirus infection blocks SARS-CoV-2 replication within the respiratory epithelium: implications for COVID-19 epidemiology. Journal of Infectious Diseases, (doi: 10.1093/infdis/jiab147) (Early Online Publication)
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236452.pdf - Accepted Version
Available under License Creative Commons Attribution.
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236452Suppl.pdf - Supplemental Material
Available under License Creative Commons Attribution.
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Abstract
Virus-virus interactions influence the epidemiology of respiratory infections. However, the impact of viruses causing upper respiratory infections on SARS-CoV-2 replication and transmission is currently unknown.
Human rhinoviruses cause the common cold and are the most prevalent respiratory viruses of humans. Interactions between rhinoviruses and co-circulating respiratory viruses have been shown to shape virus epidemiology at the individual host and population level. Here, we examined the replication kinetics of SARS-CoV-2 in the human respiratory epithelium in the presence or absence of rhinovirus. We show that human rhinovirus triggers an interferon response that blocks SARS-CoV-2 replication.Mathematical simulations show that this virus-virus interaction is likely to have a population-wide effect as an increasing prevalence of rhinovirus will reduce the number of new COVID-19 cases.
INFECTION WITH THE COMMON COLD MIGHT PROVIDE SOME LEVEL OF PROTECTION AGAINST COVID-19
Issued: Tue, 23 Mar 2021 00:01:00 GMT
The common cold virus could offer some level of protection against COVID-19 infection, according to a new study.
The research – published today in Journal of Infectious Diseases and led by scientists at the MRC-University of Glasgow Centre for Virus Research (CVR) – found that human rhinovirus (the virus that causes the common cold) triggers an innate immune response that seems to block SARS-CoV-2 replication in cells of the respiratory tract.
In further studies, mathematical simulations by the research team showed that this virus-virus interaction might have a population-wide effect, and that an increasing prevalence of rhinovirus could reduce the number of new COVID-19 cases.
Human rhinoviruses cause the common cold and are the most widespread respiratory viruses found in people. Previous research has shown that interactions between rhinoviruses and other respiratory viruses can affect the type and severity of infections in individuals, and the way in which they infect and circulate around groups of people (patterns of infection).Viruses only infect a small number of cell types within the body, and respiratory viruses typically infect cells within the respiratory tract.In the study, the researchers first infected human respiratory cells with SARS-CoV-2 in the lab, recreating the cellular environment in which infections normally occur. They then studied the replication of SARS-CoV-2 in these cells, both in the presence and absence of rhinovirus.Professor Pablo Murcia, from the MRC-University of Glasgow Centre for Virus Research, explains: “Our research shows that human rhinovirus triggers an innate immune response in human respiratory epithelial cells which blocks the replication of the COVID-19 virus, SARS-CoV-2. This means that the immune response caused by mild, common cold virus infections, could provide some level of transient protection against SARS-CoV-2, potentially blocking transmission of SARS-CoV-2 and reducing the severity of COVID-19.“The next stage will be to study what is happening at the molecular level during these virus-virus interactions, to understand more about their impact on disease transmission. We can then use this knowledge to our advantage, hopefully developing strategies and control measures for COVID-19 infections.“In the meantime, vaccination is our best method of protection against COVID-19.”The study, ‘Human rhinovirus infection blocks SARS-CoV-2 replication within the respiratory epithelium: implications for COVID-19 epidemiology’ is published in the Journal of Infectious Diseases. The study was funded by the Medical Research Council (MRC).
And for some expert reaction:
MARCH 23, 2021
A lab study published in the Journal of Infectious Diseases suggests that infection with human rhinovirus, the virus that causes the common cold, might provide some level of protection against COVID-19.
No one should expect that a fall wave of Rhinovirus to save us from our current SARS-CoV-2 pandemic, but understanding what drives these interactions could lead to better treatments, or preventatives, against COVID-19 and other epidemics in the future.
