Since the advent of the novel coronavirus, SARS-CoV-2, numerous researchers have suggested that there are several strains and that mutations have resulted in changes in the virus’s contagious and lethal properties. Opinions, on the other hand, are split.
Is there more than one SARS-CoV-2 strain?
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Genetic mutations are a common occurrence in nature. They are possible whenever genetic material is copied.
When a virus replicates within the cell it infects, the countless new copies will all be somewhat different. Why is this critical?
When mutations alter the way a virus functions, the effects can be severe. These interactions do not have to be harmful to the host; nevertheless, in the case of vaccinations or medicines that specifically target certain viral proteins, mutations may decrease these connections.
Numerous research investigations conducted since the advent of SARS-CoV-2 have shown variations in the virus’s genomic sequence. This has sparked debate about whether or not there are several strains, whether this affects the virus’s ability to infect a host, and whether or not this has an effect on how many more individuals are likely to die.
Numerous scientists have urged caution. In this Special Feature, we outline what researchers presently know about SARS-CoV-2 mutations and hear from specialists about their perspectives on the pandemic’s implications.
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What is the significance of mutations?
SARS-CoV-2 is a single-stranded RNA virus with an envelope, which indicates that its genetic material is encoded in single-stranded RNA. It constructs its own replication mechanism within the host cell.
RNA viruses have an abnormally high mutation rate due to the proneness of their replication enzymes to make mistakes when creating new viral copies.
Prof. Jonathan Stoye, a virologist and senior group leader at the Francis Crick Institute in London, explained to Medical News Today why viral mutations are crucial.
“A mutation is a change in the sequence of a gene,” he explained. “The fact of a mutation is irrelevant; what matters are the functional consequences.”
If a particular genetic modification alters the target of a virus-fighting medication or antibody, the viral particles with the mutation will overrun those without.
“A modification in a protein that allows the virus to enter a cell with extremely low levels of receptor protein may also provide a growth advantage on the virus,” Prof. Stoye noted.
“However, it should be emphasized that only a small percentage [of] all mutations will be beneficial; the majority will be neutral or detrimental to the virus and so will not persist.”
“Virus mutations are certainly important, as demonstrated by the necessity to develop new vaccinations against [the] influenza virus each year to prevent seasonal flu effectively and the need to treat HIV-1 concurrently with several medicines to [avoid the formation of] resistant virus.” — Jonathan Stoye, Ph.D.
Mutations are discovered by researchers
MNT recently highlighted a study conducted by researchers at Arizona State University in Tempe. The article identified a mutation that replicates an occurrence that occurred during the 2003 SARS pandemic.
The researchers examined five nasal swab samples that tested positive for SARS-CoV-2. They discovered that one of them was missing a segment of the viral DNA. To be exact, 81 nucleotides were deleted from the viral genetic coding.
A previously published study revealed that comparable alterations impaired the SARS virus’s capacity to reproduce.
Another research, published in the Journal of Translational Medicine, hypothesized that SARS-CoV-2 had developed different mutation patterns in diverse geographical areas.
The researchers evaluated eight recurring mutations in 220 COVID-19 patient samples from the University of Maryland in Baltimore and the Italian biotech business Ulisse Biomed in Trieste.
They discovered three of them solely in European samples and three exclusively in North American samples.
Another study, which has not yet been peer-reviewed, shows that SARS-CoV-2 mutations have increased the virus’s transmissibility in some cases.
Bette Korber and colleagues from New Mexico’s Los Alamos National Laboratory identify 13 mutations in the area of the viral genome that encodes the spike protein in the study.
This protein is required for infection because it assists the virus in attaching to the host cell.
The researchers observe that one specific mutation, which alters an amino acid in the spike protein, “may have originated in either China or Europe, but [began] to spread fast initially in Europe, then around the world, and is now the dominant pandemic form in several nations.”
Prof. Stoye stated that the study’s findings are not surprising in certain aspects.
“Typically, viruses are highly tailored to their host species. If they switch species, for example, from bat to human, some degree of retuning is unavoidable to evade natural host defenses and to interact optimally with the new host’s cells,” he explained.
“Random mutations will occur, and the viruses that are the most adapted will eventually dominate,” he continued. “It is therefore unsurprising that SARS-CoV-2 is developing as a result of its introduction into and dissemination across the human population. Clearly, such changes are occurring now, as demonstrated by Korber [and colleagues apparent ]’s spread of the [mutation].”
Prof. Stoye, on the other hand, believes that it is unclear at the moment how mutations will influence the long-term behavior of SARS-CoV-2.
“Fears that SARS-CoV-2 would evolve to become resistant to yet-to-be-developed vaccines and treatments are not unreasonable,” he added. “However, like with the so-called seasonal coronaviruses, it is feasible that we may witness evolution toward a less dangerous variant of the virus.”
Opinions continue to be split.
Earlier this year, researchers from Peking University in Beijing, China, released a study in the journal National Science Review identifying two different SARS-CoV-2 lineages they dubbed “S” and “L.”
They examined 103 viral sequences and concluded that about 70% were of the L lineage.
However, a team from the University of Glasgow’s Center for Virus Research disagreed with the findings and published a criticism of the data in the journal Virus Evolution.
“In light of the implications of these assertions and the widespread media coverage of these sorts of publications, we have thoroughly evaluated the data given […] and shown that the paper’s key findings cannot be substantiated,” the authors write.
Prof. David Robertson, head of the Centre for Virus Research’s Viral Genomics and Bioinformatics division, was a member of the team. MNT inquired about his thoughts on the likelihood of more than one strain of SARS-CoV-2.
“Until we see evidence of a change in the virus’s biology, we cannot conclude that new strains of the virus exist. It’s critical to understand that mutations are a natural consequence of virus replication and that the majority of changes we see will have no effect on the virus’s biology or function,” he explained.
“While some of the findings of, for example, amino acid alterations in the spike protein are intriguing, they are at best hypotheses at the time. Their potential influence is being evaluated in a variety of laboratories.”
Prof. Stoye believes that it is now “more a matter of semantics than anything else.”
“If our sequences differ, we have distinct strains. It makes sense to categorize the various isolates only when we have a better grasp of the functional ramifications of the observed evolutionary changes,” he explained.
“At that point, we may investigate the relationship between sequence variation and prognostic or therapeutic implications. This may take several years.”
Serotypes and directions for future study
Therefore, what proof are skeptical scientists seeking in the dispute over numerous SARS-CoV-2 strains?
Prof. Martin Hibberd of the London School of Hygiene and Tropical Medicine in the United Kingdom was invited by MNT to weigh in on the topic.
“For virologists, the term strain is more of a subjective term that does not necessarily have a clear, precise definition,” he explained.
“More relevant in the SARS-CoV-2 situation is the concept serotype,’ which is used to characterize strains that can be differentiated by the human immune response — an immune response to one serotype often does not protect against another serotype. There is yet no clear proof that this has occurred in the case of SARS-CoV-2.”
“To demonstrate that the virus has evolved sufficiently genetically to elicit a distinct immune response, we would need to define the immunological protection and demonstrate that it was effective against one serotype but not another,” he said.
Prof. Hibberd, who has been studying SARS-CoV-2 mutations, stated that scientists are investigating neutralizing antibodies to aid in the definition of a SARS-CoV-2 serotype. While these antibodies are efficient in preventing the virus from infecting a host cell, they may be ineffective against a novel strain.
“Several organizations worldwide have found a particular mutation in the SARS-CoV-2 spike protein, and they are afraid that it may affect this form of binding, but we cannot be certain at the present. More likely, this mutation will impact the virus’s ability to attach to its receptor […], thereby impairing transmissibility.” — Martin Hibberd, Prof.