An Unpredictable Virus

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By Nancy Heneson

WELL, HERE we are, still stumbling down the Midway at the carnival of angst we call the third decade of the twenty-first century, courtesy of the virus known as SARS-CoV-2.

Snippets of genetic code clothed in protein, viruses are among Nature’s strangest inventions—not quite alive yet somehow driven to reproduce. Devoid of intention yet easy to anthropomorphize as the lowest criminals of the microbial world, they hijack living beings’ cellular machinery for the sole “purpose” of making more of themselves, and leave their hosts in a range of conditions, from unharmed to chronically ill and disabled to dead.

Whatever these critters’ unique oddities, humans have had quite enough of them; it’s well past time for the scary Funhouse to shut down, the fire-eaters and bearded ladies to retire, and the Hall of Mirrors to cease distorting and politicizing facts. We are tired and cranky and want to go home.

Sensing the unrest, the message factory has begun to send out murmurs of reassurance: As the virus evolves it will become less deadly and eventually endemic, like the flu—manageable with a yearly vaccine and lethal to only 1 percent or so of the world population.  May we exhale now?

Not yet, say the experts. To be able to accept these somewhat discouraging words, we first need a little lesson in evolutionary theory. When considering evolution, it’s common to think of the phrase “survival of the fittest.” And that’s unfortunate, because this phrase is deeply misunderstood. “Fittest” does not mean strongest, swiftest, best looking or even richest (though access to resources does play a role). It means two other things: fitting best into a particular environment and leaving more offspring than other, less fit, competitors.

Example: Big, strong, lumbering bull frogs versus scrawny, speedy little bull frogs. When the mating game is afoot, the half-pound weaklings have the advantage—they can zoom around their larger and clumsier competitors and reach the females first, inseminating them with their scrawny bullfrog genes and assuring continuation of the variety, variety being the key word here.

What fuels evolution is genetic variation, i.e., mutations that change an organism’s ability to negotiate an environment. Sometimes mutations are advantageous; sometimes they kill before the organism can reproduce, and often they come bearing mixed blessings. Think of sickle cell disease: This genetic mutation in the shape of red blood cells originally occurred in areas where malaria cut a wide swath of destruction. The sickling trait destroyed the malarial parasite and in most cases still allowed the red cells to carry sufficient oxygen throughout the body; thus, the carriers survived and passed on the mutation. However, in environments without malaria, the gene confers no advantage, and if both parents pass it on, the child is likely to have serious disease.

Back to the virus: Covid has already proven its ability to evolve variants. If it needs humans to reproduce, why wouldn’t the variants that severely harm or kill the host be weeded out and supplanted by milder versions? Remember the frogs?  They got in and got out, leaving their packet of genes with the obliging female. Even if a bigger frog later stomped them to death (just a thought), they would still have fulfilled their destiny.

Similarly, the covid virus only needs human DNA long enough to reproduce and be transmitted, and as it may take two or three weeks for people to die from covid, the virus is already well on its way through the air to the next victim. Viruses don’t care about collateral damage.

Further, as Professor David Robertson of the University of Glasgow’s Centre for Virus Research pointed out in a recent interview with The Guardian, “if another variant pops out in six months, it could be worse…. It’s important not to assume that there’s some inevitability for Omicron to be the end of Sars-CoV-2’s evolution.” And even if Omicron reaches a ceiling as it runs up against more vaccinated people (the concept of herd immunity), it could create a space for a virus that’s better at evading the immune response, Robertson concludes.

What then, can we hang on to for some sort of reassurance? Enter Johns Hopkins public health expert Dr. Joshua Scharfstein. He does not dispute the unpredictability of the evolutionary course of the virus. He does, however, offer perspective. In a recent online interview with Congressman John Sarbanes (D-MD), Scharfstein reminded us that the large majority of new severe covid cases are among the unvaccinated. In addition, he said, “a lot of virus [such as from a super spreader] is what makes you sick.”

These two facts can guide us toward appropriate strategies for defense against the current variant(s) and probable future ones. It all goes back to Dr. Fauci’s three cardinal rules:  mask up, stand back and wash your hands, slightly redefined now as double mask, avoid crowds, and most important, get vaccinated and boosted. Though Emmanuel Macron has been quoted as wanting to make life miserable for the unvaccinated of France, we are unlikely to follow his lead in the good old USA.

Instead, says Scharfstein, when you encounter someone who refuses to be vaccinated (try to avoid them first), ask them for whom they would get vaccinated—mother, spouse, child, friend? In Scharfstein’s experience, people who finally decide to be vaccinated, whatever their reasons for formerly resisting, cite the people they care about more often than any other reason.

The National Institutes of Health also have a bit of good news. Researchers recently discovered that cannabinoids can prevent entry of live SARS-CoV-2 and its variants into human epithelial cells. Not quite the same as smoking a joint or taking some hemp extract and feeling safer, but certainly something to hope for as we prepare as best we can for when the next carnival to comes to town.

—Nancy Heneson is a freelance science writer and editor based in Baltimore, Maryland.