Like all living things, the virus that causes COVID-19 continues to evolve, illustrating why we need to understand the forces of evolution.
The SARS-CoV-2 virus likely “jumped” from a related mammal to humans via one or more random mutations in its genetic material in late 2019. It quickly demonstrated the survival and reproductive advantage of its altered genetic makeup allowing it to exploit a new host’s vast population. That’s evolution through natural selection.
Public health authorities designated the gene sequence of the first SARS-CoV-2 samples as “alpha.” Because of its less stable, single-stranded gene structure compared to the double-stranded structure of other viruses and other organisms, SARS-CoV-2 alpha quickly acquired new genetic mutations. That led to the ongoing parade of SARS-CoV-2 variants and subvariants.
If the single-stranded genetic structure of SARS-CoV-2 is loosey-goosey, its reproductivebehavior is even worse.
SARS-CoV-2 outsourced reproduction to more than 100 million American hosts whose cells were commandeered to make billions of new viruses. In the process, it has killed over 1.1 million of those hosts and over 6.74 million globally. It continues to do so.
Viruses like SARS-CoV-2 need not bother with the fuss and muss of sex. They can still gain the evolutionary benefit of sexual reproduction — genetically variable offspring — through mutation or recombination with other viral strains invading a host at the same time.
As a dual-infected host cell cranks out copies of both viruses, it can include genes from both parent lineages in newly produced viruses. Some of those recombinant viruses succeed well relative to other SARS-CoV-2 variants in their environment. The omicron subvariant XBB appeared through this recombination process last year.
XBB’s new, recombined genes decreased host antibodies’ ability to attach and destroy it.Nonetheless, XBB was only so-so at getting into host cells.
An apparently new, random mutation rendered XBB better at entering host cells giving rise to the XBB.1.5 subvariant first sequenced four months ago in the northeast United States. One World Health Organization official called XBB.1.5 “the most transmissible variant that has been detected yet.”
As of one week ago, the XBB.1.5 subvariant caused half of all new COVID-19 cases in theUnited States. It caused over 85% of new cases in the Northeast, and it caused 24% of new cases in the Midwest, including Ohio. The XBB.1.5 subvariant likely will continue to increase its contribution to new COVID-19 infections in the United States.
While highly transmissible, omicron XBB.1.5 does not appear to cause more severe infections than other variants. Immunity from infection with earlier variants of SARS-CoV-2 or the original vaccines targeting them likely provide little immunity to omicron XBB.1.5 due to its array of mutations. The newer bivalent booster targets omicron and provides some level of immunity to it, especially for older adults.
Vaccine resistance by SARS-CoV-2 variants; antibiotic-resistance by disease-causing microbes; herbicide-resistance by targeted weeds; and insecticide-resistance by disease-carrying mosquitoes arise predictably through evolution via mutation, recombination and natural selection.
It’s easy to think they are out to get us. They’re not. They just are the best of their kind at surviving and reproducing at our expense.
We need to understand that. We need to teach that in our schools. We need to build that insight into our public policies.
Steve Rissing is professor emeritus in the Department of Evolution, Ecology and Organismal Biology at Ohio State University.
steverissing@hotmail.com