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What you need to know about the future of variants




Over the past year, SARS-CoV-2 variants have overturned the best plans for recovery. As I write, the global spread of Delta variants obscures the prospect of an early end of the pandemic. Delta has surpassed the alpha mutant in recent months, overtaking it as the most prevalent strain of SARS-CoV-2 infection (Figure 1). Virologists disagree with the following question: Are Deltas as devastating as they come, or are they even more powerful variants on the horizon?

Some argue that the SARS-CoV-2 repertoire is limited. Others, including myself, believe that viruses have the potential for more changes than we have ever seen. Optimists focus on the repetition of independent mutations in peplomers as evidence of limited potential for change. If that is true, a widespread defensive vaccine may be right there. These non-optimistic views look at the failure to create a pan-protective influenza vaccine that requires annual re-vaccination to keep pace with influenza variants.

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Eventually we will get the answer. Until then, we can only try to understand SARS-CoV-2 in more detail, both through a thorough study of the virus itself and the similarities that we know from studies of other viruses. I still have little knowledge of answering questions because I have all the great tools at my disposal, but I’m struggling to report that what we know is a concern.

A quick examination of the SARS-CoV-2 mutant revealed that the non-peplomer region of the genome had the same number of mutations (nucleotide changes) as the peplomer itself (Fig. 2). Many of these mutations can affect the structure and function of viral genes in addition to peplomer. Almost all discussions about variants ignore or reject the potential association of these mutations. Given what we know about viral replication and pathological subtleties, this seems like a serious oversight. The point is the subtle differences between the pathogenicity of polio and the genome of the vaccine.The decisive difference between pandemic stocks Poliovirus The live attenuated vaccine, the Sabin vaccine, is a single nucleotide modification that does not alter a single amino acid.

Recently paper By Thorne et al. Repeat the imminent risk warning. Researchers have found that mutations in alpha variants that alter a single amino acid in the N protein gene result in 80-fold overexpression of the Orf9b messenger RNA duplication gene. The authors attribute the overproduction to a fundamental change in the nucleotide sequence that dramatically increases the relative abundance of Orf9b messenger RNA, rather than a significant change in N protein function. They also speculate that overproduction of the Orf9b protein may enhance the transmission and lethality of Alpha mutants. Why? The Orf9b protein contributes to the suppression of innate immunity, which can increase the time it takes for the virus to replicate before immune recognition interferes with its progression. It is worth noting that another suppressor of innate immunity, Orf6, is also overexpressed by the Alpha variant. Why remains a mystery.

Understanding the epidemiology of alpha variants and the contribution of mutations to their pathogenesis is like looking through a glass in the dark. There is a lack of important information about SARS-CoV-2 to guide us. Similarly, there is a lack of detailed information on the structure and function of HIV that guides our ability to develop new drugs to prevent and treat AIDS infection. Lack of investment in coronavirus research impedes the ability to predict where and how the next variant will appear. One remedy is to dramatically increase the budget for basic research on coronavirus. This is a successful strategy to defend HIV in 1985. Another remedy is to look for clues to other well-studied viruses. This is three examples from studies of three different viruses, showing that subtle genomic mutations can have unexpected effects on viral replication and pathogenesis.

Example 1.. Most influenza vaccines today are the preparation of dead viruses made from large batches. Vaccine scientists have found that fragments of the viral genome are complete throughout the virus, dramatically reducing virus yields. There was ongoing competition to understand what was advantageous for replicating these fragments over the entire genome. Scientists were surprised when they tracked down the causes of changes in some single amino acids in the viral NS2 gene. Until then, it was not thought to function solely to remove viral RNA from the nucleus and play a direct role in genomic replication.

Example 2.. In an attempt to adapt a particular strain of hepatitis C to the growth of cell culture for research purposes, Chan et al. Strains that replicate 1000 times higher in cell culture than their parents were isolated. Further analysis revealed that the cause was subtle amino acid changes in six viral proteins, including structural and nonstructural proteins. The main contribution was due to the nonstructural protein, which stabilizes the half-life of free viral particles and increases them by a factor of 3-4. However, the sum of the individual contributions to the increase in infectivity was smaller than that of the ensemble.

Example 3.. The third example is from another coronavirus that causes hepatitis in mice. In trying to understand the signals needed to generate new copies of the viral genome, researchers introduced mutations that largely eliminated the ability of the virus to grow. Eventually, a rapidly growing strain emerged despite the detrimental mutation. They then sought to discover how the virus overcame its disadvantages. The answer was completely surprising. It was caused by mutations in the genes encoding viral proteins, NSP8 and NSP9. These two genes are far from the site of the original mutation. Experiments have revealed a previously unexpected role for these two proteins in viral replication.

The lessons learned from the study of SARS-CoV-2 mutants are clear. Studies focus on including studies of all other proteins, both single and multiple combinations, from studies of peplomer alone to viral replication in tissue culture and organoids, as well as the ability to avoid immune recognition. Need to spread.

These three examples illustrate the complexity and subtleties associated with understanding viral infections and increased pathogenicity. Don’t underestimate the virus’s enemies. Our watchword must be alert, not complacent, until we know much more than we know today about the basic aspects of coronavirus replication, etiology, and mutation. A much more contagious and dangerous virus than Delta may be in progress.





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