New variants are always popping up as we have noted previously. Nature has a brief note on the P.1 variant from Brazil. It notes:
A coronavirus variant detected in the Brazilian city of Manaus might be driving reinfections and the city’s second wave of COVID-19. During the first wave of the pandemic, Manaus experienced one of the world’s highest infection rates: an estimated two-thirds of residents were infected by October 2020, leading some researchers to predict that population-wide immunity might cause new infections to tail off. But in January 2021, researchers identified a novel coronavirus variant, called P.1, during a period of rising hospitalizations in the city and linked the variant to a few cases of reinfection. To characterize the variant further, Nuno Faria, at Imperial College London, and his colleagues analysed viral genomes collected from 184 human samples in Manaus between November and December (N. R. Faria et al. Preprint at https://github.com/CADDE-CENTRE/Novel-SARS-CoV-2-P1-Lineage-in-Brazil/blob/main/manuscript/FINAL_P1_MANUSCRIPT_25-02-2021_combined.pdf; 2021). The variant harbours 17 mutations that alter SARS-CoV-2 proteins. Among the alterations are changes in the SARS-CoV-2 spike protein that have been previously linked to increased transmission and immune evasion.
From the referenced paper the authors note:
Lineage P.1 contains 10 new amino acid mutations in the virus spike protein (L18F, T20N, P26S, D138Y, R190S, K417T, E484K, N501Y, H655Y, T1027I) compared its immediate ancestor (B.1.1.28). In addition to the abovementioned estimated increase in the rate of molecular evolution during the emergence of P.1, we find, using molecular selection analyses, evidence that 9 of these 10 mutations are under diversifying positive selection .Three key mutations present in P.1, N501Y, K417T and E484K, are located in the spike protein RBD. The former two interact with human angiotensin-converting enzyme 2 (hACE2), whilst E484K is located in a loop region outside the direct hACE2 interface. Notably, the same three residues are mutated with the B.1.351 variant of concern, and N501Y is also present in the B.1.1.7 lineage. The independent emergence of the same constellation of mutations in geographically-distinct lineages suggests a process of convergent molecular adaptation. Similar to what was observed for SARS-CoV-1, mutations in the RBD may increase affinity of the virus for host ACE2 and consequently impact host cell entry and virus transmission. Recent molecular analysis of B.1.351 suggests that the three P.1 RBD mutations may similarly enhance hACE2 engagement, providing a plausible hypothesis for an increase in transmissibility of the P.1 lineage. Moreover, E484K has been associated with reduced antibody neutralisation and as RBD-presented epitopes account for ~90% of the neutralising activity of sera from individuals previously infected with SARS-CoV-2, tighter binding of P.1 viruses to hACE2 may further reduce the effectiveness of neutralizing antibodies that are competing with hACE2 to bind the RBD. However, it remains difficult to estimate the contributions of the P.1 RBD mutations to transmissibility and neutralisation that may have led to P.1’s emergence at the population level.
Grinch reports the following SNPs:
aa:orf1ab:S1188L
aa:orf1ab:K1795Q
del:11288:9
aa:S:L18F
aa:S:T20N
aa:S:P26S
aa:S:D138Y
aa:S:R190S
aa:S:K417T
aa:S:E484K
aa:S:N501Y
aa:S:H655Y
aa:S:T1027I
aa:orf3a:G174C
aa:orf8:E92K
aa:N:P80R
New Jersey reports 2 cases in Hudson County. However this variants seems to attacks specific ACE2 receptors. It is more virulent and its control and mitigation is critical. Hopefully this does not start the process all over again!
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