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Evolution of SARS-CoV-2 variant

Evolution of SARS-CoV-2 variant

 


Recent articles published in Cold Spring Harbor Perspective in Medicine We have demonstrated the evolutionary process and biology of coronavirus 2 (SARS-CoV-2), a severe acute respiratory syndrome that is the causative agent of the coronavirus disease 2019 (COVID-19) pandemic.

Research: Evolution and biology of SARS-CoV-2 mutants. Image Credit: GEMINI PRO STUDIO / Shutterstock
study: Evolution and biology of SARS-CoV-2 mutants.. Image Credit: GEMINI PRO STUDIO / Shutterstock

Background

SARS-CoV-2, an enveloped positive-strand plus RNA virus, was first identified in December 2019 in Wuhan, China. Later, the emergence of the virus was related to Wuhan’s South China Seafood Market, and the first genomic sequence data of the original Wuhan strain was released on January 10, 2020. Due to the proliferation of cases around the world, the World Health Organization (WHO) has declared SARS-CoV-2. A pandemic occurred on March 11, 2020.

The alpha variant of SARS-CoV-2 (first detected in the UK in December 2020) is the first identified variant of concern (VOC), beta (South Africa, December 2020), gamma ( Brazil, January 2021), followed by Delta. (India; May 2021), and Omicrons (South Africa; November 2021) variants.

SARS-CoV-2 is one of the deadly members of the human betacoronavirus family. Other members are Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV) and Middle East Respiratory Syndrome Coronavirus (MERS-CoV). The Phylogenetic analysis SARS-CoV and SARS-CoV-2 have been shown to emerge from different SARS-related coronavirus strains. SARS related coronavirusThe subgenus Salvecovirus and the genus Betacoronavirus are found in animals such as horseshoe-shaped bats, pangolins, and civets.

Spike glycoproteins on the surface of SARS-CoV-2 play an important role in viral entry. This protein has two subunits, S1 and S2. The receptor binding domain (RBD) of the S1 subunit binds to the host cell’s receptor angiotensin converting enzyme 2 (ACE2) and initiates the viral entry process. The furin cleavage site at the S1 / S2 junction plays an important role in viral entry.

Evolution of SARS-CoV-2

The evolution of the virus is primarily caused by mutations that make it easier for the virus to escape existing host immunity and adapt to new hosts. Mutations that have emerged in the SARS-CoV-2 genome during evolution have repeatedly increased their transmissibility and antigenic escape capacity.

In SARS-CoV-2, most of the mutations Spike protein.. The ability of peaplomers to accumulate large numbers of mutations may be due to their plasticity due to relaxed structural constraints.

The D614G amino acid substitution of the spike protein is the first mutation to significantly increase the infectivity of SARS-CoV-2. This was followed by an N439K mutation in the spike receptor binding motif (RBM), which also increased SARS-CoV-2 transmissibility, antigenic escape capacity, and fitness for replication.

In 2020, the virus evolved relatively slowly compared to other respiratory viruses. Alpha VOCs, first identified in the United Kingdom in December 2020, showed several mutations in pesplomers believed to result from chronic infections in immunocompromised patients. All subsequent VOCs (beta, gamma, delta, and omicron) show numerous mutations, and the omicron variant shows the most spike mutations compared to previous VOCs. These VOCs are evolving in countries with high infection rates and demonstrate the role of existing host immunity as a positive selective pressure for viral evolution.

Factors that cause the evolution of viruses

SARS-CoV-2 replication is driven by RNA-dependent RNA polymerase and additional error-correcting enzymes. This error-correcting enzyme is responsible for high replication accuracy compared to other respiratory viruses. It is unclear whether SARS-CoV-2 has undergone a temporary or gradual evolution, but chronic infections in immunocompromised patients are transient SARS- when new mutants emerge. It is generally considered to be the main driver of the evolution of CoV-2. ..

In addition to chronic infections, a series of infections in areas with high infection rates could be another powerful driver of the evolution of SARS-CoV-2. It is possible that both drivers are working together to generate different sublineages. One example could be an infection in a community involving several immunocompromised patients.

Genetic recombination between divergent variants has been observed during the evolution of SARS-CoV-2. However, these recombinant variants most often show lower community transmission rates compared to novel variants with new escape mutations. These mutations act as a force of adaptive evolution, significantly enhancing the transmission, immunity, and pathogenicity of life.

Impact of evolution of SARS-CoV-2

Most of the SARS-CoV-2 mutants that appeared before Omicron show increased infectivity. Omicron variants are the first VOCs characterized by both transmission fitness and antigen discontinuous mutations, significantly improving immune fitness.

Increased binding affinity for host ACE2 is believed to be the main reason for the increased transfer rate. However, increased viral load in the airways due to improved replication suitability and antigenic escape can also play a potential role.

A significant reduction in pathogenicity has been observed in the recently emerged Omicron mutants. This may be due to a decrease in the endogenous pathogenicity of the mutant, as well as the induction of adaptive immunity at the population level by infection or vaccination.

Regarding the immune response to SARS-CoV-2 infection, studies have shown that viral variants are less likely to escape the memory T cell response in individuals who already have immunity to SARS-CoV-2. However, most mutants, including Omicron, are highly effective in evading antibody-mediated neutralization.

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