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Peculiar evolution of the Monkeypox virus genomes

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We compare the evolution of 14 genomes of monkeypox viruses including that of May 2022 that is currently spreading among humans in numerous countries outside Africa. Our aim was to discover mutations and other viral evolutions (recombination) of the virus genome that may explain the sudden impact of this epidemic circulating at very low-level and alert on its potential pathogenic character. We have evidenced the presence of a succession of a large number of T bases between the DNA-dependent RNA polymerase subunit rpo132 and the cowpox A-type inclusion protein, progressively rising from the absence of a characteristically long pattern of T-bases found in succession (≤ 10) in the early genomes of 1971, up to the 19 T-base sequence in the Israel 2018 reference strain and the 30 T bases thereafter in the 2022 strains. We find a complementary match for this long sequence of T bases only in the simian hemorrhagic encephalitis virus, at the 3’ end of the genome with a long succession of 28 A-bases after the stop codon. More strikingly, we find that the corresponding 10 phenyl-alanine aa chain is reported as matching uniquely (E≤0.001) a hypothetical protein element in Plasmodium falciparum, Yersinia pestis, Escherichia coli and Penicillium nordicum. We wonder whether this region of the monkeypox genome situated right upstream this long T-repeat may potentially code for a not yet identified polypeptide sequences with a functional role.


Monkeypox virus, biomathematics, master code, evolution, genomics, proteomics