Does SARS-CoV-2 Trigger Stress-InducedAutoimmunity by Molecular Mimicry? A Hypothesis

Francesco Cappello; Antonella Marino Gammazza; Francesco Dieli; de Macario; Alberto Jl Macario

doi:10.3390/jcm9072038

Does SARS-CoV-2 Trigger Stress-InducedAutoimmunity by Molecular Mimicry? A Hypothesis

J Clin Med. 2020 Jun 29;9(7):2038. doi: 10.3390/jcm9072038.

Authors

Francesco Cappello^{1

2}, Antonella Marino Gammazza¹, Francesco Dieli¹, de Macario^{2

3}, Alberto Jl Macario^{2

3}

Affiliations

¹ Department of Biomedicine, Neuroscience and Advanced Diagnostics (BIND), University of Palermo,90127 Palermo, Italy.
² Euro-Mediterranean Institute of Science and Technology (IEMEST), 90141 Palermo, Italy.
³ Department of Microbiology and Immunology, School of Medicine, University of Maryland at Baltimore-Institute of Marine and Environmental Technology (IMET), Baltimore, MD 21202, USA.

Abstract

Viruses can generate molecular mimicry phenomena within their hosts. Why shouldsevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) not be considered one of these?Information in this short review suggests that it might be so and, thus, encourages research aimingat testing this possibility. We propose, as a working hypothesis, that the virus induces antibodiesand that some of them crossreact with host's antigens, thus eliciting autoimmune phenomena withdevasting consequences in various tissues and organs. If confirmed, by in vitro and in vivo tests,this could drive researchers to find effective treatments against the virus.

Keywords: COVID-19; SARS-CoV-2; antistress proteins; cell stress; crossreactive antibodies; molecular chaperones; molecular mimicry.