The coronavirus SARS-CoV-2 has constantly evolved since it was first detected in humans over a year ago. Viruses replicate exceedingly fast, and each time they do, there’s a small chance they mutate. This is par for the course, if you’re a virus.
But in the last few weeks, scientists have been investigating SARS-CoV-2 variants with a handful of mutations arising much faster than expected. Normally, we’d expect to see one to two largely inconsequential genetic changes in the coronavirus every few months. New variants are emerging with a constellation of mutations, all at the same time.
In December 2020, the UK announced a variant of coronavirus, and two other variants were later detected in South Africa and Brazil. There is, for the time being, no reason to fear these variants or how the coronavirus is mutating — scientists and the World Health Organization suggest that our current protective measures of social distancing and masking up work just as well against them. However, scientists are closely monitoring and evaluating them because they could worsen the pandemic if they are more transmissible or can evade our immune system and vaccines.
Epidemiologists, virologists and immunologists are now tasked with understanding how these mutations in the new variants may change the virus and how our bodies respond to them. Mutations could change SARS-CoV-2 in such a way that it may even be able to evade the immune response generated by vaccines. Preliminary research shows our current vaccines should be able to deal with the three most concerning variants, but data continues to roll in.
Scientists can see the virus evolving in real time and are in a race to describe how this evolution might affect our immunity and, down the line, treatments and vaccines. Here, we’re sharing everything we know about COVID-19 variants and the various esoteric ways scientists discuss mutations and evolution.
How does the coronavirus mutate?
The coronavirus is an RNA virus, which means its complete genetic sequence, or genome, is a single-stranded template (humans and other mammals, by contrast, use double-stranded DNA). The template of SARS-CoV-2 is made up of four bases — denoted by the letters a, c, u and g — in a specific sequence, about 30,000 letters long.
The template provides instructions on how to build all the proteins that make a new coronavirus particle. To replicate, SARS-CoV-2 needs to take over a host cell and use it as a factory, hijacking the machinery within. Once it sneaks into a cell, it needs to read the RNA template.
Critical to this process is an enzyme known as an RNA-dependent RNA polymerase, or RdRp. It has one job, and it’s terrible at it. “This is an enzyme that makes a huge amount of mistakes when replicating,” says Roger Frutos, a molecular microbiologist at the French Agricultural Research Centre for International Development, or CIRAD. The RdRp introduces errors during replication, producing new viruses with slightly different templates. Changes in the template are known as mutations.
Mutations often have little effect on a virus, but sometimes they change the template so much they cause changes in the virus’ physical structure. “A mutant doesn’t mean it’s like 10 times scarier or 10 times deadlier,” says Tyler Starr, a computational biologist at the Fred Hutchinson Cancer Research Center. “Mutations have incremental effects.”
This could be a bad thing for SARS-CoV-2, creating a useless zombie virus. Sometimes, it might confer an advantage, like allowing the virus to bind more…
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