Viruses move a fine line between harmfulness and transmissibility. If they are too virulent, and as a result they kill or incapacitate their hosts, their ability to infect new ones is limited. Conversely, if viruses do little harm, they may not make enough copies of themselves to be infectious.
But SARS-CoV-2, the coronavirus that causes COVID-19 disease, does not meet this norm for evolutionary balance. Symptoms often do not appear until after those infected have been spreading the virus for several days. A study on SARS-CoV-2 found that the highest rates of viral shedding (and therefore transmissibility) occurred a day or two before the infected person showed symptoms.
To put it simply, you only feel sick when the virus has already achieved its evolutionary goal: to spread.
Viruses that have a high capacity to make copies of themselves and then introduce them into new carriers are more efficient and have higher prevalence levels, and therefore take longer to be held back by group immunity or health efforts.
As academic researchers studying evolutionary medicine, we know that the balance between harmfulness and transmissibility helps keep a pathogen under control. For a virus, lethality is something that prevents it from spreading excessively. This has been the case for other pandemic pathogens such as the Marburg virus, Ebola or the original coronavirus responsible for SARS. Outbreaks that consistently cause severe symptoms are easier to corner through public health measures, as infected individuals are easier to detect. However, SARS-CoV-2 can secretly infect entire communities because many of those infected do not have any symptoms at all.
COVID-19 behaves like an STD
Seen from this perspective, COVID-19 is reminiscent of a sexually transmitted disease. The infected person shows no symptoms and continues to feel fine… and while still spreading the virus. AIDS and syphilis, for example, are relatively asymptomatic diseases for most of the time they are contagious. With regard to SARS-CoV-2, there is recent research that maintains that between 40% and 45% of infected people remain asymptomatic. And these carriers may have the ability to spread the virus for longer.
COVID-19 has another similarity with many sexually transmitted diseases, and that is that its perniciousness is not the same in all hosts. In fact, it is often extremely variable. There is scientific evidence that the ability to defend against infection varies from person to person. Furthermore, the severity of all strains of the virus may not be the same, although there is not yet sufficient scientific evidence on the latter.
Even within the same strain of SARS-CoV-2, the virus could affect hosts in different ways, which in turn could facilitate its spread. Neither SARS-CoV-2 (nor any other pathogen) deliberately changes its effects to take advantage of us and use our bodies as vehicles of transmission. But pathogens can evolve to look like they are playing games with us.
There are studies that show that pathogens can regulate the virulence with which they manifest (which means that they can be extremely virulent in some individuals and much less in others) depending on characteristics of the host such as age, the presence of other infections or your immune response. In some individuals, virulence would be maximized, as in the case of older hosts. In others, what would be maximized would be transmissibility.
Age matters
So far, it seems that age is the fundamental factor. Older people tend to suffer from highly damaging infections while younger guests, despite being equally infected, mostly emerge unscathed. This could be because different hosts develop different immune responses. Another answer would be that, as we get older, we are more susceptible to developing other diseases such as obesity or hypertension, which in turn make us more prone to harmful effects from SARS-CoV-2.
Regardless of how exactly it works, being governed by age patterns allows SARS-COV-2 to suck and puff at the same time in evolutionary terms, that is, to wreak havoc among the oldest hosts with great virulence and preserve the younger ones for that serve as a transmission vehicle. Some studies suggest that young people are more susceptible to being asymptomatic, although both presymptomatic and asymptomatic can still spread the virus.
What do we know about the evolution of SARS-CoV-2? Unfortunately, not too much yet. There is some scientific evidence that the virus could be adapting to us as new hosts, but so far there is no evidence to show that these mutations are causing changes in the virulence or transmissibility of SARS-CoV-2. And since the virus might be able to circumvent the typical balance between perniciousness and transmissivity, there might be little evolutionary pressure for it to become less harmful in its spread.
Of all the mysteries surrounding COVID-19, one thing is clear: we cannot get carried away by a false sense of security. As Sun Tzu warns in The Art of War , you have to know your enemy. And we still have a lot more to know about SARS-CoV-2 before we start claiming victory.
By Athena Aktipis, Center for Medicine and Evolution (Arizona State University) and Joe Alcock, University of New Mexico.
This article was originally published on The Conversation. Read the original.
