It will take time for the virus to reach significant genetic diversity. Sars-CoV-2 mutates fairly slowly for a virus, with each line acquiring one a few changes every month;; two to six times lower than the number of mutations that influenza viruses acquired over the same period.
Yet mutations are the foundation upon which natural selection can act. Most often, mutations render a virus inoperable or have no effect at all.
However, there is the potential for mutations to affect the transmissibility of Sars-CoV-2 in its new human hosts.
As a result, intense efforts have been made to determine which of the mutations identified since the first Sars-CoV-2 genome was sequenced in Wuhan can significantly alter virus function.
A notorious mutation in this context is an amino acid change in the Sars-CoV-2 spike protein, the protein that gives coronaviruses their characteristic crown-like projections and enables them to attach to host cells.
This single change in character in the viral genome is known as D614G – It has been shown to increase viral infectivity in cells grown in the laboratory, without having any measurable effect on the severity of the disease.
Although this mutation is also found almost systematically in three other mutations and all four are now found in around 80% of the sequenced Sars-CoV-2s, it is the most common group of mutations in the circulation.
The challenge with D614G, as with other mutations, is to unravel whether their frequency has increased because they happened to be present in viruses responsible for sowing previously successful outbreaks, or whether they are present really give an advantage to their bearers.
While genomics is working on a UK dataset, this suggests a subtle role for D614G in increasing the Growth rate of lines wearing it might find our own job no measurable impact when transferring.
Simply taken with you
D614G isn’t the only mutation found at high frequency. A number of three mutations in the protein envelope of Sars-CoV-2 are increasingly appearing in sequencing data and are now found in a third of viruses.
A single change at position 57 of the Orf3a protein, a known immunogenic region, occurs in a quarter.
Other mutations exist in the spike protein, while myriad others appear to be induced by the activity of ours own immune response.
At the same time, there is no consensus that these or others significantly change the transferability or virulence of viruses. Most mutations are simply carried along as Sars-CoV-2 continues to spread successfully.
However, replacements aren’t the only small changes that can affect Sars-CoV-2.
It was shown that there are deletions in the Sars-CoV-2 minor genes Orf7b / Orf8 Reduce the virulence from Sars-CoV-2, which may cause milder infections in patients.
A similar Deletion may have behaved in the same way in Sars-CoV-1, the related coronavirus that was responsible for the Sars outbreak in 2002-04.
Progressing to a less virulent Sars-CoV-2 would be welcome news, although deletions in Orf8 have been around since the beginning of the pandemic and are no longer occurring.
While adaptive changes may still occur, all data currently available suggest that we have faced the same virus since the beginning of the pandemic.
Chris Whitty, Chief Medical Officer for England, rightly poured cold water on the idea that the virus got mutates into something milder than the one that led Britain to impose a lockdown in March.
Possible decreases in symptom severity over the summer are likely due to infection in younger people, containment measures (such as social distancing), and improved treatment rather than changing the virus itself.
While Sars-CoV-2 hasn’t changed much to this day, we continue to expand our tools to track and track its evolution to keep up.
Lucy van Dorp, Senior Research Fellow, Microbial Genomics, UCL
This article is republished by The conversation under a Creative Commons license. read this original article.