Mutating coronavirus: what it means for all of us
An important milestone in the fight against COVID-19 was early January 2020, when the entire viral genome of the novel coronavirus that caused the disease was sequenced for the first time. Since then, the entire coronavirus genome, extracted from thousands of infected patients around the world, has been sequenced.
This huge bank of genome sequences is an important resource. Especially since viruses such as the corona virus have a high mutation rate, with the genome sequence varying up to 0.02%. This may sound quiet, but considering that the human genome varies by only 0.001% between individuals, it is clear that the virus mutates much faster than we do and can develop quickly.
Sequencing the coronavirus at different times can tell us how it adapts and can indicate the direction in which it is likely to go.
In a recent study, the London School of Hygiene and Tropical Medicine (LSHTM) analyzed the viral genome sequences that were isolated from over 5,000 COVID-19 patients around the world. What does this analysis of genome variations tell us? What is the impact on vaccines, treatments and tests? And what does it tell us about the future direction of this destructive pathogen?
All viral vaccines contain material that resembles the virus they want to protect against. This fakes the immune system to develop a response and produce antibodies that are ready to use if they ever encounter reality. In the case of corona virus, the immune system produces antibodies that target the spike protein - the part of the virus that is used to penetrate our cells.
One worry is that the virus mutates to form "escape mutants". These are mutated versions of the virus that the vaccine-induced antibodies do not recognize. We see this with other viruses like influenza. The flu vaccine needs to be changed every year to counter changes in circulating strains.
Fortunately, the novel coronavirus has a lower mutation rate than influenza. And while the LSTHM study identified changes in the S gene (the tip gene) of the various virus strains, mutations in this gene were comparatively rare. Mutations in the epitope regions (the sites in the spike protein where the antibodies attach) were also rare.
The first searches for an effective treatment focused on existing medications, according to recent reports on the success of dexamethasone. While this drug prevents a hyperactive immune response to the virus, other promising drugs like remdesivir target the virus itself. Remdesivir specifically targets the enzyme that the virus needs to replicate.
Previous studies found two mutations in the enzyme gene that confer resistance to remdesivir, but the LSHTM study did not find many cases of these mutations. However, widespread use of the drug will put selective pressure on the virus (environmental factors that contribute to evolutionary change). Monitoring of these mutations is therefore important.
To diagnose a current infection, diagnostic tests look for specific genes of the virus. The accuracy of these tests depends on how the target areas of the genome are as expected.
The first published diagnostic method, which was published shortly after the sequencing of the first viral genome, was examined for more than one viral gene which is considered to be "well preserved" across virus strains. (Well-preserved genes are important to the functioning of the virus and therefore do not change as the organism develops.) Most diagnostic tests have continued to look for two or more coronavirus genes, although the genes they test for are common vary.
The authors of the LSHTM study looked for variations in regions of the genome that were examined in common diagnostic tests and found several mutations that could lead to "false negative" results in which a person suffers from the disease, but the test says that this is not the case. These mutations had a wide geographic distribution, so clinical scientists need to consider the locally circulating strains when considering which tests to use.
Similarly, once restrictions on international travel are relaxed, scientists need to watch out for possible false negatives in imported diseases.
Diagnostic tests look for specific coronavirus genes. They are not looking for a genome-wide match. Exposure visualizations
More or less deadly?
Some viruses that cross the species barrier in humans are poorly equipped to multiply in their human hosts and cannot remain present in the human population. However, the corona virus has already achieved sustained human-to-human transmission. But will this presence be maintained? And if so, will the virus develop more or less fatally?
Like mutations in any organism, a viral mutation must offer an evolutionary advantage for it to prevail. There is no evolutionary advantage for a virus if it kills its host, especially if it kills the host before it is transferred to a new one. However, causing symptoms in the infected person, such as coughing and sneezing, can help the virus to spread to a new host, and this offers an evolutionary advantage.
To find out which mutations can help the virus survive, the authors of the LSHTM study aimed to identify "convergent mutations" - mutations that occurred in different parts of the world and at a higher than random rate, what was on it suggests that these mutations benefit survival from the virus.
Although scientists have analyzed many genomes, the investigation of the relationship between genome and disease is still in progress. Unfortunately, there is a bias in the genome sequence database because samples from patients with more severe symptoms are more likely to be sequenced, making it difficult to link certain mutations to the severity of the disease.
Of course, the disease outcomes are also influenced by other factors, e.g. B. how old or sick the host is. The impact of interventions must also be taken into account. Until a large data set of genome data from mild or non-symptomatic patients from a different population is available, it will be difficult to derive how the identified convergent mutations affect the severity of the disease.
This article is republished by The Conversation under a Creative Commons license. Read the original article.
Claire Crossan receives Covid19-related research funding from Xenothera Ltd.
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