Virologist explains what you need to know about new coronavirus variants

Infectious disease expert Dr. Dave Wessner explains why it is so important to identify new variants of the coronavirus that causes Covid-19 as they emerge.

Despite all the upbeat news about coronavirus vaccines, other current news about Covid-19 is more sinister. Detection of a genetic variant of SARS-CoV-2, initially in the UK and now in other countries around the world, has raised troubling questions. Is this new variant, called B.1.1.7, more transmissible? Could it lead to an explosion of new cases and further strain healthcare systems? Could vaccines less easily neutralize this new variant? To fully assess these concerns, we can explore what we know about viral replication and analyze the lessons learned from other viruses.

The appearance of viral variants is not unusual.

The appearance of variants of SARS-CoV-2 is not surprising at all. Viruses mutate. Much. In fact, numerous studies have shown that viruses mutate at a much higher rate than multicellular organisms, such as humans. Also, viruses replicate very quickly. When a virus particle enters a host cell, it turns it into a viral factory, spewing out thousands of new virus particles in a relatively short period of time. The result? A multitude of viral mutants invariably arises within an infected individual. Virologists often use the term “viral swarm” to reflect the large number of variants that inevitably occur in an infected individual.

Many of these mutants may differ genetically from the original virus, but they do not exhibit biologically important differences. Others may be inferior; that is, mutations make the virus less capable of replicating within a host or of spreading from one host to another. In some cases, however, the mutations can confer what is called a “selective advantage.” This means that a particular mutant could infect a person more easily, replicate more within the body, or even simply leave a person’s body more easily. These types of changes increase the chances that a virus will survive and reproduce, which can be worrisome in the case of more dangerous viruses.

Viral variants are not always more difficult to treat

Even compared to other viruses, the human immunodeficiency virus (HIV) mutates quite quickly. Consequently, many of its genetic variants have been categorized. In fact, geneticists have divided the predominant HIV virus into at least nine subtypes or clades. Interestingly, these variants differ in their geographic distribution. Most infections in North America, Western Europe, and Australia are caused by clade B. In contrast, clade C is much more prevalent in southern Africa and clade A is more prevalent in Russia and the former countries. Soviet Union. However, despite the genetic variety, these variants show very limited biological differences. Transmission patterns and disease progression appear to be the same for all clades. Also, existing antiretroviral therapy (ART) appears to be equally effective for all strains.

So what has driven the geographic distribution of these variants? Probably the dominance of different clades in different geographic regions is largely due to chance. If a certain variant enters a particular population, that variant could spread throughout the population, quickly becoming the dominant variant. This process probably explains the geographic distribution of HIV subtypes. Most likely, one of the first people in the United States to be infected with HIV was infected with a version of the clade B virus. As a result, this variant now accounts for approximately 90% of all HIV infections in the United States. USA

Some viral variants can evade existing treatments

The high mutation rate of viruses, to some extent, explains why people can become infected with the flu repeatedly and why we need a new flu vaccine every year. The virus mutates. As a result, the structures of proteins on their surface change, a process known as antigenic drift. Although each individual mutation probably will not significantly alter protein structures, a combination of mutations can change molecular structure significantly. Our immune system no longer recognizes the virus. The vaccine loses its effectiveness. To combat these molecular changes, researchers use various algorithms to predict which variants of influenza will predominate in the next year. These variants, then, form the basis of the new vaccine.

Mutations sometimes lead to the appearance of new viruses.

Dog owners have probably heard of canine parvovirus (CPV). This virus is quite transmissible between dogs and can have serious consequences. Fortunately, an effective vaccine exists, and vaccinated dogs are largely resistant to infection. Despite its current worldwide distribution, CPV did not exist 50 years ago; it is actually a variant of feline panleukopenia virus (FPV). At the genetic level, CPV and FPV differ only slightly, but those differences have dramatic consequences. FPV can infect cats, mink, and raccoons. But it cannot infect dogs. In contrast, CPV can infect dogs, but not cats.

In this case, random mutations led to the evolution of a new virus. The genetic code of FPV, which replicates in a cat (or other permissive animal host) changed, and as a result, the exterior of the virus changed, which meant that unlike its predecessors, this FPV variant could infect the dog. The virus replicated in this new host and spread to other dogs. Thus, a new virus emerged that quickly spread throughout the world.

Certain Variants of SARS CoV-2 Concern Public Health Officials

Although coronaviruses generally mutate less rapidly than influenza or HIV viruses, SARS-CoV-2 has been mutating during the Covid-19 pandemic. In fact, at the beginning of the pandemic, one particular variant, dubbed D614G, quickly replaced the initial strain of SARS-CoV-2 around the world. This strain contains a change in the “spike protein” of the virus that allows it to be more easily transmitted from one host to another. Due to this biological difference, the strain spread rapidly.

So why is variant B.1.1.7 causing such concern? The answer is multiple. First, the sequence analysis of B.1.1.7 provided by the UK’s Covid-19 Genomics Consortium shows that it differs quite a bit from other SARS-CoV-2 variants. Although there are only a few mutations among the variants, B.1.1.7 exhibits a number of changes. Some researchers have postulated that it may have arisen in an immunosuppressed or immunosuppressed individual. In a person with a weakened immune system, the virus could replicate for a long time. During this period, a number of individual mutations could accumulate. The result? A virus like B.1.1.7. So that virus could have been passed on to someone else. In other words, the individual mutations occurred in a fragmented fashion. But the researchers did not detect these intermediaries. The mutated virus was not detected until it was transmitted to another person.

Second, several of the mutations present in B.1.1.7 exist in the gene encoding the coronavirus spike protein. Changes in this protein could alter the effectiveness of recently developed vaccines. All major vaccines in development focus on this critical molecule. Mutations in the gene that encodes the spike protein could alter its structure and these changes could affect the effectiveness of vaccines. Studies designed to explore the effectiveness of existing vaccines against this new variant are underway.

Finally, this variant appears to be more transmissible than other variants. First identified in September 2020, B.1.1.7 caused 60% of new coronavirus infections in London in mid-December. More recently, it has been detected in numerous countries, including the United States. A rigorous scientific analysis of its transmission properties is underway.

The appearance of this variant of SARS-CoV-2 and its rapid spread is undoubtedly noteworthy. At a very basic level, a more detailed understanding of its evolution and biological properties could provide us with important insight into the pathogenesis of Covid-19. More immediately, monitoring both this and other variants that are sure to emerge is crucial to our ongoing efforts to reduce the pandemic.

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