Right now, it’s convenient to think of the SARS-CoV-2 virus as having three properties: How contagious is it? How virulent is it? And how evasive is it? That last one is a measure of how well the virus avoids being shut down either by the immune response generated by vaccines, or by the existing antibodies left behind by past infection.
Over time, as the number of people vaccinated gets closer to that magic “herd immunity” number (a number that gets higher, as the virus gets more contagious), the the first value and the third value will become almost synonymous. That is, in a society where almost everyone has been either vaccinated or had the disease, the best measure of how contagious the virus is will be closely defined by how evasive it is.
But we’re not there yet. The number of vaccinated people in the U.S. may be growing rapidly, with around a quarter of all adults vaccinated at the moment. However, that’s not nearly enough for vaccination to be a major factor in the virus’ ability to spread. If we keep vaccinating, we’ll get there.
But when considering the connection between contagion and virulence, there’s just one thing to know: There pretty much isn’t one. Or at least, there’s not one in the way most people would like to believe.
In almost all cases, there is absolutely no evolutionary pressure that would cause a disease to become less deadly over time. Sure, it might be easy to believe that a virus which is 100% deadly would eventually wipe out its host species, and that such a disease would either have to moderate its virulence or disappear along with whatever creature was so unfortunate as to be infected.
Tell that to smallpox. Throughout a run that goes back at least to Egyptian tombs in the third-century BCE, hemorrhagic Variola major maintained a case fatality rate between 90-100%. For all forms of the disease, the case fatality rate never fell below 30%. If you caught smallpox, your odds of dying from it were extraordinarily high.
Why didn’t everyone die of smallpox? Well, a lot of people did; about 300 million people in the 20th century alone. That is not a value that represents “getting less deadly with time.”
One big reason even more people didn’t die from smallpox is because smallpox evolved to get more deadly. Somewhere around 3-4,000 years ago (based on genetic evidence), the virus that causes the worst form of smallpox emerged, by evolution through what would have been initially a variant on another virus. That virus, possibly Variola minor, remained in circulation, so people who caught that virus developed a degree of immunity to the more deadly variety. Smallpox was extremely contagious and horrendously virulent … but not all that evasive, thank God.
There exist in nature viruses that are highly contagious, almost certainly fatal, and so evasive that even past infection with the same virus doesn’t provide immunity. These viruses are controlled by a drop in contagion. That doesn’t happen because the virus gets weaker. It happens when it has killed enough of a local community that there’s no one left to spread the virus. This is not the preferred method of getting transmission numbers down. Fortunately, none of these viruses is currently prevalent in humans.
So … back to the SARS-CoV-2 virus.
The whole reason this virus is known as the SARS-CoV-2 virus is because it’s extremely similar to the virus that causes SARS. The case fatality rate for SARS is estimated at 15%. So we can all be grateful that COVID-19 doesn’t match the virulence of its older sibling. But does this mean that the virus has already gotten weaker? No.
It’s a change in contagion that represents the big difference between the two. On paper, SARS appears to be as contagious as COVID-19 when comparing the two in identical situations. But there’s one very big difference: Patients infected with SARS-CoV don’t really spread the virus effectively until a day or two after symptoms appear, while patients infected with SARS-CoV-2 hit their peak rate of infection almost coincident with the appearance of symptoms, and are infectious in the days before symptoms appear. That’s it. That’s the big evolutionary advantage that the new virus gained over the older form: It can infect people more easily, because people who are pre-symptomatic can spread the virus without yet knowing they have it. That doesn’t seem to be the case with SARS.
There are situations where a virus can evolve a variant where a change in virulence affects the rate of contagion. A virus that kills its host so quickly that its unable to spread effectively is an unfit virus, in an evolutionary sense. It won’t succeed against variants that allow the host to carry. But there are very real limits on this, and they don’t come anywhere close to the claim that “viruses get less deadly over time.”
The pressure that exists on viruses is simply to become more contagious. The version of a virus that spreads most rapidly wins. For the most part virulence does not enter the picture. For SARS-CoV-2, the period of peak infection is in that initial week after infection, with very few cases of transmission occurring after the first two weeks. The virus could be 100% fatal after that point, without making much impact on its ability to spread. There’s no evolutionary pressure for the virus to become more virulent. There’s also precious little for it to become less virulent.
Right now, SARS-CoV-2 is a highly successful virus. After all, despite its high rate of death, the SARS-CoV virus only managed killed something like 850 people worldwide. More people died of SARS-CoV-2 in the United States today.
Why? Because viruses do not automatically get less deadly over time.