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Thursday, March 25, 2021

Catch a Cold!

For some idiosyncratic reason, we started feeling superstitious about wishing someone "good luck" and instead expressed it contrarily by saying "Break a leg." Contrarily, we often say to someone "Be well," "Stay safe," or similar. Why don't we instead implore them to "catch a cold?"

Some say "The best defense is a good offense." That is an old idiom of questionable origin. The point of it is that attacking your foe will consume its attention, thus leaving it less resource or attention to engage in attacking you. In a similar vein, it is sometimes possible for some foe's resources to be consumed by some other entity or force, thus resulting in a similar depletion of the foe's resources but without your effort. The old idiom for this is "my enemy's enemy is my friend." Idioms can be illuminating.

The offense and enemy idioms came to mind recently as I read a new article recently published in The Journal of Infectious Diseases, jiab147. Scientists in the United Kingdom have been studying the manner in which viral infections interact with one another. Specifically, they were interested in the relationship between the common cold (rhinovirus) and SARS-CoV-2 (which causes COVID-19). Their conclusion is that "this virus-virus interaction is likely to have a population-wide effect."

Without a doubt, there are steps that humans can take to protect against SARS-CoV-2/COVID-19. For the last year, we have heard about hand washing, not touching our face, and social distancing. For months, we have heard about mask-wearing though that has been a bit of a rollercoaster. For weeks now, we have heard about vaccines available to prevent the most serious effects of COVID-19. Each of these represents an effort we can exert. And, once inoculated, the vaccine can exert some effect of its own.

The UK research identifies an ally though; an enemy of an enemy. It is not new. The researchers note that previous studies have demonstrated that the common cold (rhinovirus) infection can stimulate the body to protect against the flu. Similarly, the rhinovirus has demonstrated some success in attenuating the severity of influenza.

The common cold has demonstrated the ability to help us defend ourselves against other viral infections. The cold has been a challenge forever, and despite herculean efforts, we as yet know of no cure. In recent years, however, we have heard promising news of progress against these pesky respiratory infections.

In 2020, there was discussion of the common cold and T-cells. The National Institute of Health (NIH) reported that our bodies can effectively learn to defend themselves against the cold virus using t-cells. That same "pre-existing T-cell memory against common cold coronaviruses can cross-recognize SARS-CoV-2." In other words, some people had a head start in resisting the novel coronavirus or in minimizing its symptomatology. In short, having had past colds assisted some of us with dealing with the exposure to SARS-CoV-2.

The new research is even more promising though. The UK scientists examined the manner in which SARS-CoV-2 replicated. The success of any virus is in its ability to invade some host and to then replicate. The simplicity of that model is then challenged if more than one virus is in competition in the same host. And, there is some hope that the common cold, while not our friend by any means, may be a less dangerous enemy than the SARS-CoV-2. Furthermore, that cold is a selfish friend that may help us ward off COVID-19 or even evict it once it has taken up residency.

That said, there is also an incidence discussion that is valid. It is noteworthy that the last year of hand washing, distancing, masking, and more have been largely successful against COVID-19. But, all of those efforts have also been largely successful against the cold and flu also. Thus, the opportunities to study SARS-CoV-2 interacting with influenza or rhinovirus have been limited. So, the UK scientists introduced these to each other in the laboratory.

What they found was intriguing. The Rhinovirus stimulates the production of interferon as a defense. And, the scientist noted that when both rhinovirus and SARS-CoV-2 were present there was a "block in SARS-CoV-2 replication." Though the virus that causes COVID-19 entered the human tissue, it was not successful multiplying. The presence of the rhinovirus was beneficial in that it does not tolerate the presence of the other virus. It inspires our immuno-response more readily and thoroughly than the SARS does. This is good news for people who have colds.

So, rhinovirus "infection impairs SARS-CoV2 replication and spread." Better news, however, is that the rhinovirus entering the body impacts COVID-19 "even . . . 24 hours after SARS-CoV-2." One can be infected with SARS-CoV-2, and catching a cold within 24 hours can be beneficial! Thus, there is a body of research developing that supports the "incurable" common cold may be more of a benefit to us than the nuisance we have always perceived.

The cold stimulates our immune systems in a more profound manner than the flu or SARS-CoV-2. Our reaction to the cold, the interferon, is effective against these and other viruses. And, as we learned early in the COVID-19 experience, our bodies' learned cold response with T-cells has the potential to help us react to new, "novel," coronaviruses to some degree. In short, the much-maligned common cold may be our best friend.

Sure, no one wants a cold. But, who wants a broken leg? Perhaps we learn to live with SARS-CoV-2 as it has come to call. Perhaps our futures bode well for ongoing habitual hand washing and vaccines. But, let me part with this wish to you - catch a cold!