Abstract
The battle against the new coronavirus that continues to kill millions of people will be still long. Novel strategies are demanded to control infection, mitigate symptoms and treatment of COVID-19. This is even more imperative given the long sequels that the disease has on the health of the infected. The discovery that S protein includes two ankyrin binding motifs (S-ARBMs) and that the transient receptor potential vanilloid subtype 1 (TRPV-1) cation channels contain these ankyrin repeat domains (TRPs-ARDs) suggest that TRPV-1, the most studied member of the TRPV channel family, can play a role in binding SARS-CoV-2. This hypothesis is strengthened by studies showing that other respiratory viruses bind the TRPV-1 on sensory nerves and epithelial cells in the airways. Furthermore, the pathophysiology in COVID-19 patients is similar to the effects generated by TRPV-1 stimulation. Lastly, treatment with agonists that down-regulate or inactivate TRPV-1 can have a beneficial action on impaired lung functions and clearance of infection. In this review, we explore the role of the TRPV-1 channel in the infection, susceptibility, pathogenesis, and treatment of COVID-19, with the aim of looking at novel strategies to control infection and mitigate symptoms, and trying to translate this knowledge into new preventive and therapeutic interventions.
Highlights
COVID-19, a new human respiratory disease that continues to kill millions of people, is a worldwide public health challenge
These studies should be corroborated by the genetic characterization of patients with COVID-19 by six nonsynonymous functional polymorphisms of transient receptor potential vanilloid subtype 1 (TRPV-1) (K2N rs9894618, P91S rs222749, I315 M rs222747, T469I rs224534, T505A rs17633288, and I585V rs8065080), that determine a substantial difference in capsaicin sensitivity with levels of SNPbased responsiveness ranging from 2 to 6
The battle against the new coronavirus will be still long, so know the mechanisms of TRPV-1, a receptor involved in lung defense mechanisms, inflammation, and immunomodulation might be relevant in the susceptibility to SARS-CoV-2 infection
Summary
COVID-19, a new human respiratory disease that continues to kill millions of people, is a worldwide public health challenge. Our recent data [38] indicate that signals from airways sensory nerves (i.e., DEP which directly activate TRPV-1 and endogenous mediators such as prostaglandin E2 (PGE2) and bradykinin (BK) which are considered to be indirect sensitizers of the channel), when they joined the central nervous system (CNS) can affect the autonomic impulse to the heart (Figure 2) All this evidence postulates a proof of concept that explains the indication that peaks of pollutants are associated with short-term cardiovascular adverse events in susceptible subjects, as for example COVID19 patients. High levels of PM in air pollution, such as DEP, directly interact with TRPV-1 (gray arrow) by modulating its activity and increasing its sensitization This interaction could worsen the outcome of COVID-19 disease in affected patients. TRPV-1 genetic variants by increasing the functional properties of the channel could render people more susceptible to virus access into the cell
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