Lack of Molecular Mimicry between Nonhuman Primates and Infectious Pathogens: The Possible Genetic Bases

Abstract

Recently, it was found that proteomes from poliovirus, measles virus, dengue virus, and severe acute respiratory syndrome-related Coronavirus 2 (SARS-CoV-2) have high molecular mimicry at the heptapeptide level with the human proteome, while heptapeptide commonality is minimal or absent with proteomes from nonhuman primates, that is, gorilla, chimpanzee, and rhesus macaque. To acquire more data on the issue, analyses here have been expanded to Ebola virus, Francisella tularensis , human immunodeficiency virus-1 (HIV-1), Toxoplasma gondii , Variola virus, and Yersinia pestis . Results confirm that heptapeptide overlap is high between pathogens and Homo sapiens , but not between pathogens and primates. Data are discussed in light of the possible genetic bases that differently model primate phenomes, thus possibly underlying the zero/low level of molecular mimicry between infectious agents and primates. Notably, this study might help address preclinical vaccine tests that currently utilize primates as animal models, since autoimmune cross-reactions and the consequent adverse events cannot occur in absentia of shared sequences.

Keywords: autoimmunity; cross-reactivity; infectious agents; molecular mimicry; nonhuman primates; peptide sharing; preclinical test; rhesus macaque; vaccines.

Fig. 1

Heptapeptide sharing between mammalian proteomes and: ( A ) F. tularensis membrane protein/O-antigen protein, ( B ) T. gondii apical membrane antigen 1-like protein, ( C ) variola virus surface antigen S, ( D ) Y. pestis virulence-associated V antigen, ( E ) Ebola virus proteome, and ( F ) human immunodeficiency virus (HIV)-1 proteome.