ArticleArXiv2021
Review of the mechanisms of SARS-CoV-2 evolution and transmission.
Article in ArXiv, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Authors and funding
3 authors.
Funding
Abstract
The mechanism of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) evolution and transmission is elusive and its understanding, a prerequisite to forecast emerging variants, is of paramount importance. SARS-CoV-2 evolution is driven by the mechanisms at molecular and organism scales and regulated by the transmission pathways at the population scale. In this review, we show that infectivity-based natural selection was discovered as the mechanism for SARS-CoV-2 evolution and transmission in July 2020. In April 2021, we proved beyond all doubt that such a natural selection via infectivity-based transmission pathway remained the sole mechanism for SARS-CoV-2 evolution. However, we reveal that antibody-disruptive co-mutations [Y449S, N501Y] on the spike protein receptor-binding domain (RBD) debuted as a new vaccine-resistant transmission pathway of viral evolution in highly vaccinated populations a few months ago. Over one year ago, we foresaw that mutations on RBD residues, 452 and 501, would "both have high chances to mutate into significantly more infectious COVID-19 strains". Mutations on these residues underpin prevailing SARS-CoV-2 variants Alpha, Beta, Gamma, Delta, Epsilon, Theta, Kappa, Lambda, and Mu at present and are expected to be vital to emerging variants in the future. We anticipate that viral evolution will combine RBD co-mutations at these two sites, creating future variants that are about ten times more infectious than the original SARS-CoV-2. Additionally, two complementary transmission pathways of viral evolution, i.e., infectivity and vaccine resistance will prolong our battle with COVID-19 for years. We predict that RBD co-mutation sets [A411S, L452R, T478K], [L452R, T478K, N501Y], [L452R, T478K, E484K, N501Y], [K417N, L452R, T478K], and [P384L, K417N, E484K, N501Y] will have a high chance to grow into dominating variants due to their high infectivity and/or strong ability to break through current vaccines, calling for the development of new vaccines and antibody therapies.
Indexed as
Identifiers
34545334PMC8452100What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.