As the coronavirus pandemic has cleared over the U.S.In addition to following the quantity of COVID-19 cases day by day, there is a worldwide scientific community engaged in tracking the SARS-CoV-2 virus itself.
For an infection, spreading for a couple of months and arriving at in excess of 3 million hosts is quite a long time to advance and change.
Some infections – like influenza – transform a great deal, we need to update vaccines yearly to remain on top of the spread of seasonal flu.
In the interim, the coronavirus that has caused the current COVID-19 pandemic has remained generally steady, and it seems to be mutating much more slowly than influenza.
So its mean coronavirus transmission will be slow compared to influenza.
It does not mean that coronavirus will not mutate.
This is great news for coronavirus treatment, vaccine development and for the scientists who are closely studying the virus. But that doesn’t mean it’s not mutating at all.
Two new studies have recently been released analysing SARS-CoV-2 mutations.
One study, from Arizona State University, discovered a large DNA deletion in a virus sample taken from a patient in Tempe.
The second study, currently still a pre-print from the Los Alamos National Laboratory, tracked mutations throughout the outbreak, and hypothesised that one strain of the virus is more infectious than the original Wuhan strain.
The Arizona study generated three full-length SARS-CoV-2 genomes from a series of samples; they found that one of these genomes, which they’ve named AZ-ASU2923, had a large deletion – 81 DNA base pairs – in a gene called ORF7a.
The ORF7a gene creates an accessory protein, which helps the virus infect, replicate and spread inside the human host.
Specifically, the protein is thought to help the virus to evade our immune system and kill the cell once the replication process is complete.
The ASU virology team had been set up to perform research on seasonal flu viruses, but when the 3rd case of COVID-19 was found in an Arizona individual on January 26, 2020,
They knew they had all technical and scientific prowess to rapidly pivot to examining the spread of SARS-CoV-2.
“This was the scientific opportunity of a lifetime for ASU to be able to contribute to understanding how this virus is spreading in our community,” said Lim.
“As a team, we knew we could make a significant difference.”
SARS-CoV-2 viral genomes.
All the positive cases show that the SARS-CoV-2 viral genomes were different from each other, meaning they were independent from each other.
This indicates that the new cases were not linked to the first Arizona case in January, but the result of recent travel from different locations.
In the case of the 81-base pair mutation, because it has never been found before in the GISAID database, it could also provide a clue into how the virus makes people sick.
It could also form a new starting point for other scientists to develop antiviral drugs or formulate new vaccines.
SARS-CoV-2 makes accessory proteins that help it infect its human host, replicate and eventually spread from person to person.
The genome deletion removes 27 protein building blocks, called amino acids, from the SARS-CoV-2 accessory protein ORF7a.
The protein is very similar to the 2003 SARS-CoV immune antagonist ORF7a/X4.
The ASU team is still studying for further information.
The ASU team is now hard at work performing further experiments to understand the functional consequences of the viral mutation.
The viral protein is thought to help SARS-CoV-2 evade human defenses, eventually killing the cell.
This frees up the virus to infect other cells in a cascading chain reaction that can quickly cause the virus to make copies of itself throughout the body, eventually causing the serious COVID-19 symptoms 8-14 days after the initial infection.
The good thing is that researchers are on the case, and we’ll no doubt have more information soon.
So, although an already dangerous and highly contagious virus mutating sounds incredibly nerve-wracking, don’t stress too much.
Viruses will mutate, and the coronavirus is no exception.
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