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RESEARCH PRODUCT

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

Francesco CappelloFrancesco DieliAntonella Marino GammazzaEverly Conway De MacarioAlberto J. L. Macario

subject

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)virusesantistress proteinslcsh:Medicinecrossreactive antibodiesWorking hypothesismedicine.disease_causeIn vivo testsViruscell stre03 medical and health sciences0302 clinical medicinecell stressAntigenmedicinemolecular mimicry030304 developmental biologyantistress protein0303 health sciencesbiologybusiness.industrySARS-CoV-2lcsh:Rmolecular chaperonesCOVID-19General Medicinemolecular chaperoneIn vitroMolecular mimicryImmunologybiology.proteinCommentaryAntibodybusiness030217 neurology & neurosurgery

description

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.

yearjournalcountryeditionlanguage
2020-06-29Journal of clinical medicine
10.3390/jcm9072038https://pubmed.ncbi.nlm.nih.gov/32610587