The continuing scourge of the novel SARS-CoV-2 coronavirus, which causes the dreaded COVID-19 disease seems relentless. Not only did it bring the world to its knees in unprecedented pandemic proportions, but it is also still mutating and evolving, albeit at a slower pace, as indicated by US microbiologists.

SARS-CoV-2 mutations

There are now more than a dozen versions of SARS-CoV-2 globally, as seen in this variant tracker from the New York Times, that may concern us in a variety of ways-some may offer extreme infectivity, while others are less potent. While this diverse array of SARS-CoV-2 variants may overwhelm us, given that it is nearly impossible to reach herd immunity, evidence shows that these variants present similar combinations of mutations. As such, we seem not to deal with totally distinct versions of the virus, as we initially feared.

A patient in South Africa receives a vaccine to curb the continuing spread of the SARS-CoV-2 virus.
(Photo: Photo by Jan Hetfleisch/Getty Images) A patient in South Africa receives a vaccine to curb the continuing spread of the SARS-CoV-2 virus.

These microbiologists are currently looking into how the SARS-CoV-2 is transforming and evolving as it reproduces and gets transmitted in humans. By using experimental evolution, wherein they grow varied populations of microbes that began from the same strain using similar conditions for several weeks and months. They study how antibiotic resistance changes and how infections endure. As they utilize the varying populations, the microbiologists attain a "replay of the tape of life" that allows them to study this evolution's recurrence and thereby determine how to predict it.

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They observe a pattern of convergent evolution, wherein similar traits would emerge from distinct, independent lineages while they adapt to the same environments over time. For SARS-CoV-2, full genome sequences of the viruses from several patients led us to find convergent patterns. While most are one-off mutations that would immediately go extinct, some create fresh lineages that have become more recurrent as the virus replicates and infects more people. Once the same portion of the virus mutates in varying samples worldwide and becomes recurrent, this mutation most probably encodes one adaptation that allows it to reproduce and spread.

Proof of Convergent Evolution

With an intensified genome surveillance of the coronavirus, studies have pinpointed proof of convergent evolution. In the US, seven genetically independent lineages were found to acquire a mutation at a particular point on the coronavirus' dreaded spike protein, which the virus uses to attach to human cells. This spike carries a sequence of connected amino acids, with a mutation that happens at position number 677. In the original SARS-CoV-2 virus, it is identified as the amino acid glutamine (Q).

In the six lineages, Q mutated to a separate amino acid histidine (H), and this became 677H. In the seventh lineage, Q would further mutate to yet another amino acid, proline (P). All these lineages each have a mutation called S:614G, which has been the first most remarkable change in the virus that was identified several months ago and transmitted so widely that it is now seen in about 90 percent of all infections. Microbiologists named these lineages in the US after common birds, such as "robin" or "pelican," to help differentiate and monitor them and prevent expected prejudice if they are named after the areas where they were found.

Lineages discovered outside the US have also gotten 677H, including those in Egypt, India, Denmark, and a large area in Macedonia. A new potent variant, B.1.525, likewise has 677H, just like lineages that came from B.1.1.7, considered the most troublesome variants to be spotted. The resulting worldwide rise of S:677 mutations and their quintuple growth in prevalence shows that these transformations enhance viral strength. It is speculated that S:677 borders an area in the spike protein that assists and guides the virus to intrude and infect human cells.

Drop-in New Adaptations

This is certainly not the only example of SARS-CoV-2 convergence. Spike mutations in its eight varying positions, at the very least, have been increasing around the world, seen in B.1.1.7 and other variants, such as B.1.351, P.1, and P.3. Such variants share mutation combinations, specifically at positions 18, 69-70, 417, 452, 501, 681, and a very worrisome E.484.K mutation that avoids neutralizing antibodies. More of these variants are now being reported, with mutations specifically defined to help in continuing research and studies. Media and government attention to this growing problem would certainly heighten, given its probability to increase contagiousness and evade existing vaccines.

As these discovered variants seem to be resampling mutations that are seen in other variants. As such, we can surmise that the coronavirus is running out of new adaptations. However, this doesn't discount the fact that such evolution or mutation would cease as we start herd immunity and relax restrictions. We have learned through history that viruses evolve quickly to avoid barriers to transmission as infections increase. We must keep in mind that as long as there are more infections, the bigger the chance of mutations, the more mutations that help the virus survive and exist will thrive. This is the reason why we should stop new infections. Such viral adaptations are currently changing what we know about convergent evolution.

Microbiologists call for new investments to develop an "early warning system" to identify new variants of SARS-CoV-2 and other pathogens. To achieve this, viral genome surveillance and sequencing are crucial. The U.S. is currently funneling investments to the Center for Disease Control and Prevention from the new federal stimulus package, wherein researchers can more frequently sequence and evaluate virus samples. This can be sustained by improving public health expertise and enhancing research infrastructure to decode genetic mutations and pinpoint the need for vaccine modifications.

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