Viruses mutate — meaning they change and evolve as they multiply and spread — and one of the big fears about SARS-CoV-2 is that at some point it could mutate into something even more deadly and even more contagious. Thankfully, so far that hasn’t happened. A University College London team analyzing virus genomes from more than 7,500 infected people identified 198 recurrent genetic mutations in the virus, and a lead researcher concluded, “there is nothing to suggest SARS-CoV-2 is mutating faster or slower than expected. So far we cannot say whether SARS-CoV-2 is becoming more or less lethal and contagious.”
While we shouldn’t count on it, there is a chance that mutation will work in our favor, eventually.
John M. Barry’s The Great Influenza is considered one of the most authoritative histories of the 1918 influenza pandemic. In that book, Barry discusses how the continuing mutation of that epidemic’s spectacularly lethal virus ended up saving people:
By nature the influenza virus is dangerous, considerably more dangerous than the common aches and fever lead people to believe, but it does not kill routinely as it did in 1918. The 1918 pandemic reached an extreme of virulence unknown in any other widespread influenza outbreak in history.
But the 1918 virus, like all influenza viruses, like all viruses that form mutant swarms, mutated rapidly. There is a mathematical concept called “reversion to the mean”; this states simply that an extreme event is likely to be followed by a less extreme event. This is not a law, only a probability. The 1918 virus stood at an extreme; any mutations were more likely to make it less lethal than more lethal. In general, that is what happened. So just as it seemed that the virus would bring civilization to its knees, would do what the plagues of the Middle Ages had done, would remake the world, the virus mutated toward its mean, toward the behavior of most influenza viruses. As time went on, it became less lethal.
Barry lays out numerous examples from cities in the United States and around the world and concludes, “despite aberrations, then, in general in youth the virus was violent and lethal; in maturity it mellowed. The later the epidemic struck a locality, and the later within that local epidemic someone got sick, the less lethal the influenza. The correlations are not perfect. Louisville suffered a violent attack in both spring and fall. The virus was unstable and always different. But a correlation does exist between the timing of an outbreak in a region and lethality.”
One major factor working against us compared to our unlucky ancestors in 1918 is that viruses, carried and spread by the infected, move at the speed of humanity. The 1918 influenza traveled primarily by ship and railroad, particularly carried by soldiers moving from one place to another as part of World War I. By comparison, SARS-CoV-2 traveled at the speed of air travel, roughly 575 miles per hour, from one densely populated city to another.
Previous coronaviruses, such as SARS and MERS, had higher fatality rates, but were less contagious. One would be foolish to count on a phenomenon that is a mathematical probability, not a law. But . . . if SARS-CoV-2 is a particularly dangerous combination of contagiousness and lethality, then at least some, and perhaps most, future mutations will make the virus at least somewhat less contagious and less lethal. Maybe natural mutation will make this virus easier to treat as the pandemic progresses.
Barry also makes an important point to keep in mind about the structure of viruses and mutation. Viruses have a giant “head,” attached to a long tube-like part called the sheath, stem or “stalk,”, and at the other end an end-plate with tail fibers that look a little like a spider or insect.* Most vaccines attack the head, which is the part that mutates the most — which is why vaccines are only partially effective. (Think of the flu vaccine given each winter, and how many people catch a different strain.) But the stem or stalk part of the virus doesn’t change very much from mutation to mutation.
Last year, researchers at the University of Michigan determined that some antibodies attack the stalk of the influenza virus — a much more effective way of killing the virus, and one that works upon almost all the viruses that the antibody encounters. Right now, we’ll take any treatment or potential vaccine we can get. But if we can develop either a treatment or vaccine that focuses on attacking the stalks of the coronaviruses . . . it will be like the Merrimack or the Monitor showing up for a battle with wooden ships.
*This is the structure of a type of virus called a bacteriophage; other viruses have different shapes. That said, one of the potential vaccines in development is using a bacteriophage to bring a “virus-like particle” into a person’s nasal cavity, triggering the body’s immune system to generate antibodies that would kick into action if the body encountered SARS-CoV-2. The virus-like particle will also “attach to receptors that the coronavirus would bind to, limiting potential sites for transmission.”