H2S as a potential defense against COVID-19?

Am J Physiol Cell Physiol. 2020 Aug 1;319(2):C244-C249. doi: 10.1152/ajpcell.00187.2020. Epub 2020 Jun 9.

Abstract

The outbreak of COVID-19 pneumonia caused by a new coronavirus (severe acute respiratory syndrome coronavirus 2, SARS-CoV-2) is posing a global health emergency and has led to more than 380,000 deaths worldwide. The cell entry of SARS-CoV-2 depends on two host proteins angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2). There is currently no vaccine available and also no effective drug for the treatment of COVID-19. Hydrogen sulfide (H2S) as a novel gasotransmitter has been shown to protect against lung damage via its anti-inflammation, antioxidative stress, antiviral, prosurvival, and antiaging effects. In light of the research advances on H2S signaling in biology and medicine, this review proposed H2S as a potential defense against COVID-19. It is suggested that H2S may block SARS-CoV-2 entry into host cells by interfering with ACE2 and TMPRSS2, inhibit SARS-CoV-2 replication by attenuating virus assembly/release, and protect SARS-CoV-2-induced lung damage by suppressing immune response and inflammation development. Preclinical studies and clinical trials with slow-releasing H2S donor(s) or the activators of endogenous H2S-generating enzymes should be considered as a preventative treatment or therapy for COVID-19.

Keywords: ACE2; COVID-19; H2S; SARS-CoV-2; TMPRSS2.

Publication types

  • Review

MeSH terms

  • Angiotensin-Converting Enzyme 2
  • Animals
  • Antiviral Agents / therapeutic use*
  • Betacoronavirus / drug effects*
  • Betacoronavirus / pathogenicity
  • COVID-19
  • COVID-19 Drug Treatment
  • Coronavirus Infections / drug therapy*
  • Coronavirus Infections / metabolism
  • Coronavirus Infections / virology
  • Host-Pathogen Interactions
  • Humans
  • Hydrogen Sulfide / metabolism
  • Hydrogen Sulfide / therapeutic use*
  • Lung / drug effects
  • Lung / metabolism
  • Lung / virology
  • Pandemics
  • Peptidyl-Dipeptidase A / metabolism
  • Pneumonia, Viral / drug therapy*
  • Pneumonia, Viral / metabolism
  • Pneumonia, Viral / virology
  • SARS-CoV-2
  • Serine Endopeptidases / metabolism
  • Signal Transduction
  • Virus Internalization / drug effects*
  • Virus Replication / drug effects*

Substances

  • Antiviral Agents
  • Peptidyl-Dipeptidase A
  • ACE2 protein, human
  • Angiotensin-Converting Enzyme 2
  • Serine Endopeptidases
  • TMPRSS2 protein, human
  • Hydrogen Sulfide