Virus vs virus: How a humble common cold virus might help us beat COVID-19

26 April 2021

Amongst the tiresome war rhetoric that the COVID-19 debacle has spawned (which I discussed in my previous articles, COVID-19 and the media: Part 1 and The fog of the war on COVID-19), an important point has been missed: viruses are at war with each other… and quite often, their infighting – known as viral interference – benefits us.

In a previous article, Duelling coronaviruses: The intriguing possibility of cross-immunity, I discussed fascinating research suggesting that infection with one of the commonly-circulating coronaviruses that cause common cold symptoms across the globe each year, may stimulate protective immunity against SARS-CoV-2, the coronavirus associated with COVID-19.

Now, a study published in The Journal of Infectious Diseases has uncovered evidence that the humble rhinovirus, which is the most prevalent respiratory virus of humans and which also causes the common cold, may stimulate an immune response that keeps SARS-CoV-2 in check.

The study, titled Human rhinovirus infection blocks SARS-CoV-2 replication within the respiratory epithelium: implications for COVID-19 epidemiology, describes experiments in which cultured human bronchial epithelial cells were infected with SARS-CoV-2, either alone, or before or after being infected with human rhinovirus.

When the cells were infected with SARS-CoV-2 alone, the novel coronavirus began slowly replicating after 24 hours, gradually picking up speed (solid red line in figure A, below). However, when cells were exposed to rhinovirus and SARS-CoV-2 at the same time, the quantity of SARS-CoV-2 dropped dramatically, and it was undetectable after 48 hours (dashed red line in figure A) whereas the quantity of rhinovirus escalated dramatically for the first 24 hours after infection, and then gradually subsided, regardless of whether SARS-CoV-2 was present (figure B).

When cells were first infected with SARS-CoV-2, and 24 hours later were exposed to rhinovirus, SARS-CoV-2 replication increased between 24 and 48 hours after infection but then sharply decreased between 48 and 96 hours after infection (dashed red line in figure C).

And when cells were first infected with rhinovirus, and 24 hours later exposed to SARS-CoV-2, SARS-CoV-2 never had a chance; the quantity of SARS-CoV-2 rapidly declined while replication of the rhinovirus was barely affected by the presence of its rival coronavirus (figure D).

Delving into the mechanisms by which the unassuming, virtually ubiquitous rhinovirus might defeat the novel coronavirus – which has been presented as an existential threat to humanity – the researchers found that rhinovirus didn’t block the ability of SARS-CoV-2 to enter cells, but once the coronavirus was inside cells, rhinovirus prevented it from replicating by triggering the release of interferon, a powerful antiviral compound manufactured by cells that form part of our innate immune system.

The researchers then developed mathematical simulations to explore the effects that circulation of rhinovirus (HRV) in a community might have on rates of SARS-CoV-2 infection. They concluded:

Their findings go a long way toward explaining the fact that young children, who ‘catch cold’ far more frequently than adults, have been observed to be at low risk of SARS-CoV-2 infection and extraordinary low risk of developing COVID-19:

Their findings also point to a potentially devastating unintended consequence of physical distancing, obsessive personal and surface hygiene, mask-wearing, and other non-evidence-based policies that have been implemented to try to ‘stop the spread’ of SARS-CoV-2: If these measures actually succeed in reducing the transmission of contagious respiratory viruses, including rhinovirus and endemic coronaviruses, they may leave us at much higher risk of suffering serious outcomes from SARS-CoV-2 infection.

Put simply, we need to allow common respiratory viruses to freely circulate through our homes and schools, in order for our immune systems to respond appropriately to novel viruses such as SARS-CoV-2.

It has become increasingly evident to me as the COVID-19 debacle drags on, that 21st century humans are the most highly educated dimwits in our species’ 200 000 year history. If our ancient ancestors were as deficient as we are now in their powers of observation, ability to process complex information and learn from experience, and capacity to discern the trustworthy from the untrustworthy amongst them, our species would never have survived to the point where we are now comfortable enough to accept living in a kakistocracy.

Fortunately for us, our physical bodies – including our wonderfully complex and resilient immune system – evolved during tougher times, when a poorly-calibrated response to challenges could quite literally mean the difference between life and death.

To ensure our continued survival as a species, we need to shake off the ridiculous New Normal propaganda and get back in touch with the wisdom built into our bodies and souls.

We need to resume hugging, kissing, speaking to each other at close range, singing in choirs, and all the other intrinsically human behaviours that are now frowned upon or outlawed by the Covidian Cult members. And we badly need to redefine our relationship with viruses, those strange gaggles of molecules that bridge the divide between the living and non-living, whose co-evolution with us has shaped us in the most intimate ways imaginable.

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