Health Science Reviews

by Mari Clark

Well, dear readers, this article is bound to confuse or possibly terrify some of you – an effortless feat in this era of COVID-19. It all begins with a group of scientists from the University of Glasgow and the Imperial College of London deciding to test a hypothesis that involves ‘fighting fire with fire’. Naturally, it is all proverbial and the fire in question here is a virus.

Before we get to the interesting part, there is a need to briefly digress and explore the wonderful phenomenon of natural selection – which is determined by the epidemiology of the virus, or the relationship between the virus and its host. This, and pathogenicity – the ability of the virus to cause disease, are influenced by factors such as the viruses’ accessibility to the host tissue and cells, the ease of the virus multiplying within the host cells and how vulnerable the virus is to host defenses. Ultimately what this all boils down to is that natural selection favors the dominance of low-virulence virus strains; meaning that the least dangerous virus will be allowed to take up prime real-estate in the body.

With the basics covered, we can start coloring in some details regarding the world of respiratory viral infections. The rapid spread of COVID-19 and its impact on global health has clearly shown us how dire the circumstances can get if we’re caught unawares. The human respiratory tract hosts a community of viruses that includes members like the Influenza viruses A (IAV) and B (IBV), Respiratory Syncytial Virus (RSV), Human Rhinovirus (HRV) and the now infamous Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). Interactions between co-circulating but categorically different respiratory viruses can influence each other’s patterns of infection. HRV and IAV have been known to interact negatively and ‘cancel’ each other out at the individual and population level and it is even suggested that a co-circulating HRV infection was able to nip France’s 2009 H1N1 influenza outbreak in the bud. HRV hindered subsequent infection of the host with IAV. The mechanisms are not entirely known – and not the focus of today’s discussion: what is important, is the fact that it has become possible to fight a blazing inferno with a match flame – and that there were scientists curious enough to see if they could apply this to COVID-19.

Using an Air-Liquid Interface cell culture system to mimic the human airway, the scientists infected human respiratory cells with SARS-CoV-2 and HRV. The experiment was split into two parts: simultaneous and staggered co-infections, using a single infection of each virus as a control. In cells simultaneously co-infected with both viruses, the amount of SARS-CoV-2 decreased over time in comparison to single infection. Even when the cells were re-infected 24 hours later with the other virus, HRV impaired SARS-CoV-2 growth. This result was further confirmed by the lack of detection of SARS-CoV-2 when infected cells were observed under a microscope.

The scientists also used mathematical modelling to extrapolate these laboratory results to a population-wide level, showing a reduction in the number of new SARS-CoV-2 infections as the number of HRV infections increase.

Before jumping to conclusions and begging anyone with the flu to give you their germs in a crazed effort to avoid COVID-19, more research is needed to understand how a common viral infection could have the potential to disrupt the ongoing COVID-19 pandemic. But for now: stay safe, get vaccinated.

Reference

Dee, K., Goldfarb, D. M., Haney, J., Amat, J., Herder, V., Stewart, M., Szemiel, A. M., Baguelin, M., & Murcia, P. R. (2021). Human Rhinovirus Infection Blocks Severe Acute Respiratory Syndrome Coronavirus 2 Replication Within the Respiratory Epithelium: Implications for COVID-19 Epidemiology. The Journal of infectious diseases, 224(1), 31–38.