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RESEARCH PRODUCT

The Role of Molecular Chaperones in Virus Infection and Implications for Understanding and Treating COVID-19

Everly Conway De MacarioCeleste Caruso BavisottoFrancesco CappelloLetizia PaladinoAntonella Marino GammazzaAlberto J. L. MacarioAlessandra Vitale

subject

Coronavirus disease 2019 (COVID-19)CoronaviridaevirusesSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2)lcsh:MedicineReviewComputational biologyvirusmedicine.disease_causechaperonopathiesVirusEpitopeAutoimmunity03 medical and health sciences0302 clinical medicinemedicineCoronaviridaechaperonotherapy030304 developmental biologyCoronavirus0303 health sciencesbiologybusiness.industrySARS-CoV-2lcsh:Rmolecular chaperonesCOVID-19General Medicinemolecular chaperonebiology.organism_classificationMolecular mimicry030220 oncology & carcinogenesischaperonopathiebusiness

description

The COVID-19 pandemic made imperative the search for means to end it, which requires a knowledge of the mechanisms underpinning the multiplication and spread of its cause, the coronavirus SARS-CoV-2. Many viruses use members of the hosts’ chaperoning system to infect the target cells, replicate, and spread, and here we present illustrative examples. Unfortunately, the role of chaperones in the SARS-CoV-2 cycle is still poorly understood. In this review, we examine the interactions of various coronaviruses during their infectious cycle with chaperones in search of information useful for future research on SARS-CoV-2. We also call attention to the possible role of molecular mimicry in the development of autoimmunity and its widespread pathogenic impact in COVID-19 patients. Viral proteins share highly antigenic epitopes with human chaperones, eliciting anti-viral antibodies that crossreact with the chaperones. Both, the critical functions of chaperones in the infectious cycle of viruses and the possible role of these molecules in COVID-19 autoimmune phenomena, make clear that molecular chaperones are promising candidates for the development of antiviral strategies. These could consist of inhibiting-blocking those chaperones that are necessary for the infectious viral cycle, or those that act as autoantigens in the autoimmune reactions causing generalized destructive effects on human tissues.

10.3390/jcm9113518https://hdl.handle.net/10447/590680