We compare the evolution of 14 monkeypox virus genomes til that of May 2022 that is currently spreading across humans in numerous countries outside Africa. Our aim was to discover mutations or other viral evolutions (recombination) that may explain the sudden impact of this very low-level circulating epidemic or alert on a potential peculiar pathogenic character. We have evidenced the presence of a large number of T bases in succession, at the level of the polymerase, 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 in succession (≤ 10) in the early genomes of 1971, up to 19 T-bases in the Israel 2018 strain of reference, and 30 T bases thereafter in the 2022 strains.
We find a complementary match for this long T bases sequence only in the simian hemorrhagic encephalitis virus, at the very 3′ end of the genome after the stop codon, with a long succession of 28 A bases. 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 about the possibility that this region of the monkeypox genome may potentially code for a not yet identified polypeptides with a functional role situated right upstream this long T-repeat.