Explained: Are new Covid-19 variants detected in the US more contagious? – The Indian Express

In a study posted on Sunday that is yet to be peer-reviewed, researchers have reported seven new variants of the SARS-CoV-2 virus in the US. Researchers are tracking virus variants since some of them might be more deadly than the original virus, they may be more easily transmissible and can have repercussions on the effectiveness of vaccines.

B.1.1.7: This variant emerged in the UK and may be associated with an increased risk of death compared with other variants, the US Centers for Disease Control and Prevention (CDC) has said.

B.1.351: This variant emerged independently from the UK variant and was first identified in South Africa. It was also reported in the US by the end of January 2021.

P.1: This variant emerged in Brazil and is known to have 17 unique mutations. Three of them are in the receptor-binding domain of the spike protein (the spike protein, which protrudes from the surface of the virus is one of the key reasons that SARS-CoV-2 has been able to spread so rapidly and therefore, any mutations that affect the spike protein are important to understand).

The authors of the recent study say that in areas where the prevalence of the virus is high, selection pressures might have favoured the emergence of variants that evade neutralising antibodies (the proteins that prevent the virus from infecting once it is inside the body). The seven new lineages noted by the researchers have all evolved a mutation in the same genetic letter, which affects the way the virus enters the human cells. But it is not yet clear if this mutation makes these new variants more contagious and more dangerous.

Further, there are likely more variants of the virus across the world, but only genome sequencing can help determine that, which is not happening sufficiently at the moment. In a document published in late December 2020, the Ministry of Health and Family Welfare outlined some steps it will take to increase and expand genome sequencing of the virus. One of the steps outlined includes sending five per cent of the positive samples to ten regional genome sequencing labs spread across the country.

Evolution helps organisms to change in response to certain changes in the environment. The goal here is to help the organism adapt so it can survive. In the Naked Ape trilogy, zoologist Desmond Morris writes about how humans have adapted to their changing environment over the course of millions of years of evolution. For instance, he considers the effects of urban city life on humans. Morris argues that despite city life being lonely and more stressful, people flock to them because a city, acts as a giant stimulus-centre where our great inventiveness can flourish and develop.

Since viruses can only replicate within a host cell, their evolution is influenced by their hosts. This means that the virus will mutate in order to evade the defenses that its hosts put up for it.

The book, Medical Microbiology says that as compared to DNA viruses, RNA viruses (SARS-CoV-2 is an RNA virus) have much higher mutation rates, probably one mutation per genome copy. Mutations might be deleterious, neutral and occasionally, they may be favourable. The book notes that only those mutations that do not interfere with the essential virus functions can persist in a given population.

An article in Nature says that compared to the HIV virus that causes AIDS, the SARS-CoV-2 virus is changing much more slowly as it spreads.

But like humans influence the evolution in viruses, viruses too, have shaped the way humans have evolved. In a 2016 study published in the journal eLife, the authors note that the constant battle between pathogens and their human hosts has long been recognised as a key driver of evolution. In this study, the authors note that about 30 per cent of all protein (proteins help cells to perform their functions) adaptations in humans since their divergence from chimpanzees have been driven by viruses. Significantly, during epidemics or pandemics, the population targeted by a virus will either go extinct, or it will adapt.

Once a virus has entered the body of its host, in order to infect the host it starts replicating, which means making copies of its entire genetic sequence. But every once in a while, the virus makes mistakes during replication. A blog entry on the website of Harvard University, explains that these mistakes, typically a change in a single letter (each coronavirus has about 30,000 RNA letters) among the thousands in the viruss sequence, might change the properties of the viruss proteins and therefore, change its capabilities. This change is called a mutation and if it is a favourable mutation, it can give the virus a new ability that promotes its reproduction, which helps the virus to become more widespread over generations.

It is likely that such kinds of favourable mutations in the SARS-CoV-2 virus are giving rise to emerging variants. For instance, the UK variant is known to be about 25-40 per cent more infectious than the original virus.

In a comment in the journal Nature, two immunologists, Dennis Burton and Eric Topol have called for an alternative approach to pandemic preparedness. In this approach, resources should be spent on developing pan-virus vaccines that can provide immunisation against multiple strains of a virus.

This is necessary in the context of SARS-CoV-2, since it is already evolving and initial evidence shows that some of its strains are more easily transmissible, implying that as more variants of the virus emerge, vaccines that already exist could be less effective against them.

While there are hundreds of coronaviruses that are known to infect animals such as pigs, camels, bats and cats, till date, seven types of coronaviruses have been identified to infect humans. In humans, the viruses usually cause mild to moderate upper-respiratory tract illnesses such as the common cold. In the last two decades, however, more aggressive coronaviruses have emerged that are capable of causing serious illness and even death in humans. These include SARS-CoV, MERS and now SARS-CoV-2.

The first coronavirus was found to infect humans in 1965, when scientists DJ Tyrrell and ML Bynoe isolated a strain of the virus called B814 from the nasal washing of a male child who had symptoms of common cold.

Vaccine development for the first four human coronaviruses, which include HCoV-229E (one of the first strains to be described in the mid-1960s), HCoV-OC43 (discovered between mid-late 1960s), HCoV-NL63 and HCoV-HKU1 (NL63 and HKU1 both discovered in Hong Kong in early 2005) was not a priority since these cause only mild illness. It was only two decades ago when SARS-CoV was emerging in China around 2003 that the need to develop a vaccine was felt since it was the first example of a human coronavirus that could cause serious illness.

Writing in the Journal of Biomedical Science, authors note that while various forms of vaccines have been developed and tested in preclinical models for SARS and MERS, none of them have been approved by the FDA.

The answer potentially lies in the spike protein of the virus, a number of which protrude from the surface of the virus forming a crown, which gives the virus its name. The spike protein makes it easier for the virus to bind with the ACE2 receptor (both SARS-CoV and SARS-CoV-2 bind to this receptor) in human cells, after which the virus starts infecting its host. But this spike protein, which makes transmission easier, is also one reason that vaccines for SARS-CoV-2 have been developed at a faster pace compared to the previous two human coronaviruses SARS and MERS, for which an approved vaccine still does not exist.

In particular, vaccine design for SARS-CoV-2 has been made faster because the spike protein offers a larger area for the vaccine to target, making it easier for it to trigger the bodys immune system into making neutralising antibodies, the proteins that prevent the spike protein from binding with the receptor and initiating infection.

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Explained: Are new Covid-19 variants detected in the US more contagious? - The Indian Express