Part of the reason for this is because, unlike many other RNA viruses, the coronaviruses have a proof-reading mechanism that helps to reduce the number of mutations they pick up. While it is clear now that the D614G mutation appears to have been an adaptation that allowed the virus to spread more rapidly in the early stages of the pandemic, SARS-CoV-2 had relatively low levels of genetic diversity globally. It has enabled us to track the virus, how it is spreading and spot variants of concern: We have been watching COVID-19’s evolution as it happens. These sequences are being shared all over the world. One advantage we have in this pandemic compared to those in the past is the extraordinary amount of genetic sequencing of the virus from samples from infected people. It was a clarifying moment for those of us studying how the virus is evolving over time. ![]() It showed how a single mutation in the virus’s genome can affect the course of the pandemic. Over the first months of the pandemic, it quickly spread around the world to become the dominant variant of the virus by the summer of 2020. This change, known as the D614 mutation, appears to have made the virus more transmissible between individuals. It is also the most visible part of the virus to antibodies, an important component of our body’s natural defences, and so a part that our immune systems learn to detect. This is the protein that studs the outside of SARS-CoV-2 and helps it to infect our cells. This mutation changed a molecule at a single location on an important part of the virus – its spike protein. Shortly after the virus arrived in Europe it picked up a mutation at an important point in its RNA genome. Currently there a handful of these around the world – four of which have been found in the UK.īut while the emergence of these variants is worrying, it is also important to remember that SARS-CoV-2 has been picking up mutations since early in the pandemic. Even more rarely, whole clusters (or ‘constellations’) of mutations can be acquired by the virus during a single infection.Īnd when viruses with these single or constellations of mutations spread more widely through populations, they may be designated "Variants of Concern". It might make SARS-CoV-2 better at getting into cells or help it escape the immune system of the person it is infecting. Occasionally, however, one of these genetic errors brings about a change that is advantageous to the virus. Currently, we know of thousands of slightly different, but genetically distinct lineages of COVID-19 spreading around the world. Using viral genetic data, my colleagues and I have recently described this process. If these can spread to other people, they can form new variants of the virus. ![]() Others don’t alter the virus’s behaviour but are also not harmful to it. Most of these mutations do not lead to anything – they are evolutionary dead ends. Like all coronaviruses, it uses a type of genetic material called RNA, which is prone to developing errors, or mutations, as the virus replicates inside a person’s cells. She is currently a recipient of the Sir Henry Dale Fellowship, which is a joint grant scheme between the Royal Society and the Wellcome Trust.Įvery time SARS-CoV-2 – the virus that causes COVID-19 – infects someone it picks up tiny changes in its genetic code as it makes copies of itself. The aim of her group is to combine a number of different approaches to produce better predictive models of how a virus might respond to different interventions. ![]() Katrina is an evolutionary epidemiologist at the University of Oxford studying how viral infections respond to different, and often conflicting, selection pressures. Group Leader, Big Data Institute, University of Oxford
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