What have we learned so far about the mutation of the virus that causes COVID-19

In early January, the first genome of Sars-CoV-2, which was the initial virus to cause the appearance of COVID-19, came under the name ‘Wuhan-1.’

This sequence of 30,000 letters (A, T, C, and G of the genetic code) marks the beginning of the fastest possible effort to understand the genetics of this newly discovered coronavirus.

Now, more than 100,000 coronavirus genomes have been sampled from COVID-19 patients in more than 100 countries.

Geneticists around the world are looking for data to understand and answer: Where did Sars-CoV-2 come from? Since when has this virus infected humans? How did the virus mutate (and do mutations have an important effect)?

Efforts to study Sars-CoV-2, like the virus, are becoming large and global.

The term mutation itself is often associated with the image of a new, dangerous virus capable of spreading across the planet.

Mutations are persistent and sometimes erase the initial form of the virus; the initial mutation in Sars-CoV-2 has spread around the world and is almost unnoticed.

However, mutations are a natural phenomenon that occurs in any organism, including viruses.

Most of the mutations have no impact on the ability of the virus to transmit or cause disease.

A mutation simply means that a difference has occurred: a one-letter change in the genome.

The Sars-CoV-2 population was genetically essentially unchanged when it jumped to the first human host on end of 2019. Now, more than 13,000 changes have been found in 100,000 Sars-CoV-2.

However, the viruses found in the two patients differed from anywhere in the world on a different average only ten letters.

These ten letters are only a fraction of the total 30,000 letters in the virus’s genetic code. This means that all Sars-CoV-2 in circulation can be considered part of one clonal / identical lineage.

Slowly mutated

Viruses need sufficient time to acquire the genetic diversity that has an impact.

In terms of the virus, Sars-CoV-2 is slow to mutate. Every bloodline only changes twice every month; this two to six times lower than the number of mutations that occur in influenza viruses during the same period.

However, mutations are the foundation of natural selection. Generally, mutations will make a virus no longer function or no longer have any effect.

But there is the potential for mutations to affect transmission of Sars-CoV-2 in humans. Therefore, intense efforts have been made to determine which mutation from the start since the Sars-CoV-2 genome in Wuhan – if any – could significantly change the function of the virus.

The known mutation in this context is the change in amino acids in the protein spike (S) Sars-CoV-2. This protein makes the corona virus appear to have a crown and is used to attach to host cells.

This single character change in the viral genome – referred to as DG14G – has been shown to increase the proliferation and spread of virus in lab-grown cells, although without measurable impact on disease severity.

This mutation is almost always found in the other three mutations systematically, and all four are now found in about 80% of the Sars-CoV-2 sequence. This makes these four mutations the most circulating collection of mutations.

The challenge with D614G – a challenge that also exists in studying other mutations – is to ascertain whether its frequent and increased occurrence was due to this mutation in viruses that were successfully transmitted early in the outbreak, or because this mutation was actually strengthen the virus.

Although a genomic study in a data set in England shows that D614G has a role in enhancing lineage growth, our study found no measurable impact of transmission.

Pretty easy to carry

D614G isn’t the only mutation that’s frequently seen. A series of three mutations in the Sars-CoV-2 protein shell are also increasingly appearing in the data and are now found in one-third of viruses.

A single change at position 57 of the Orf3a protein, which is known to be immunogenic, was found in a quarter of viruses.

Another mutation occurs in proteins spike (S) and various other mutations appear to be caused by activity human immune response.

At the same time, there is still no agreement that this mutation, or any other, significantly alters viral transmission or malignancy. Most of the mutations just get carried away because Sars-CoV-2 continues to spread successfully.

But changes in genome lettering aren’t the only minor changes that could have an effect on Sars-CoV-2. Deletion of the Orf7b / Orf8 gene in Sars-CoV-2 has been shown to reduce violence virus, and could potentially cause a milder infection in the patient.

Deletion Likewise, it may have had the same effect on Sars-CoV-1 – the corona virus that caused the Sars outbreak in 2002-2004.

The developments regarding the weaker Sars-CoV-2 would certainly be good news, but the deletions at Orf8 occurred in the early days of the pandemic and do not appear to be increasing in frequency.

While adaptive changes may not have occurred yet, all the data available at this stage suggests that we are dealing with the same virus from the start of the pandemic.

Chris Whitty, the British government’s chief medical advisory officer, issued a statement that was true when he denied that the virus in Britain had mutate to be less impactful than the virus that caused Britain to do lockdown last March.

The symptoms of illness that appear lighter during the months of June, July and August in the UK may be due to the increasing number of young people being infected, the success of control measures such as physical distancing and better treatment.

While Sars-CoV-2 has not changed significantly to date, we are continuing to develop tools to track it. We’re ready to keep up.

Wiliam Reynold translated this article into Indonesian.

–