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Abstract
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.
Highlights
Viruses need molecules from the host cell for their survival and dissemination and molecular chaperones are among them
The purpose of this review is to survey the literature and compile examples of interactions of viruses with chaperones, focusing on information that might be relevant to COVID-19, the disease caused by SARS-CoV-2, and thereby reveal points of attack for agents aimed at preventing infection, and/or blocking the chaperone-depending pathogenic mechanisms
The host’s chaperones and their teams and networks are necessary for virus infection, survival, and spreading
Summary
Viruses need molecules from the host cell for their survival and dissemination and molecular chaperones are among them. In December 2019, the new SARS-CoV-2 associated with a severe acute respiratory syndrome, quickly spread in the city of Wuhan (China), causing COVID-19 (coronavirus disease-19), affecting over 41 million people and killing over one million worldwide, at the time of this writing (latest WHO data updated October 24, 2020) This made COVID-19 a major concern for global health [18]. SARS-CoV and SARS-CoV-2 penetrate human cells using the angiotensin-converting enzyme 2 (ACE2), while dipeptidyl peptidase 4 (DPP4) represents the access receptor for MERS-CoV Both types of receptors, which are recognized and bound by the viral spikes, are present in many tissues, such as heart, kidneys, and type 2 pulmonary alveoli [20,21,22]. The purpose of this review is to survey the literature and compile examples of interactions of viruses with chaperones, focusing on information that might be relevant to COVID-19, the disease caused by SARS-CoV-2, and thereby reveal points of attack for agents aimed at preventing infection, and/or blocking the chaperone-depending pathogenic mechanisms
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