2020
DOI: 10.1186/s10020-020-00216-9
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Abstract: Hydrogen sulfide (H2S) is a natural defence against the infections from enveloped RNA viruses and is likely involved also in Covid 19. It was already shown to inhibit growth and pathogenic mechanisms of a variety of enveloped RNA viruses and it was now found that circulating H2S is higher in Covid 19 survivors compared to fatal cases. H2S release is triggered by carbon monoxide (CO) from the catabolism of heme by inducible heme oxygenase (HO-1) and heme proteins possess catalytic activity necessary for the H2S… Show more

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Cited by 28 publications
(34 citation statements)
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“…Recently, some studies provided evidence for a potentially modulatory role of hydrogen sulfide (H 2 S) in COVID-19 (17,21,28,83,108). Intravenous administration of the antioxidant, cysteine prodrug and H 2 S donor N-acetylcysteine (NAC) led to remarkable clinical and biochemical improvement in 10 consecutive patients with severe COVID-19 (45).…”
Section: Introductionmentioning
confidence: 99%
“…Recently, some studies provided evidence for a potentially modulatory role of hydrogen sulfide (H 2 S) in COVID-19 (17,21,28,83,108). Intravenous administration of the antioxidant, cysteine prodrug and H 2 S donor N-acetylcysteine (NAC) led to remarkable clinical and biochemical improvement in 10 consecutive patients with severe COVID-19 (45).…”
Section: Introductionmentioning
confidence: 99%
“…NO acts as a vasodilator and an antiviral agent in patients with SARS and can inhibit in vitro replication of SARS-CoV-2 [9 , 10] . While several recent reviews also suggest an association between H 2 S and SARS-CoV-1/2, they provide little evidence of any of such relationship[ [11] , [12] , [13] , [14] ]. Consistent with these suppositions is the possibility that endothelial dysfunction concomitant with COVID-19 infection is likely to result in reduced NO and H 2 S metabolite availability.…”
Section: Introductionmentioning
confidence: 99%
“…In the case of COVID-19, some authors proposed that polymorphism in ACE2 gene (located on chromosome X) coding and regulatory regions may partially explain such a sex-connected variability [ 11 ]. However, other factors may be involved, possibly including biochemical patterns ruling natural defenses against viruses (for example the sex related differences in H 2 S synthesis) as well as genes involved on immune responses located on chromosome X like CD40 ligand ( CD40L ), TLR7 , TLR8 , forkhead box p3 ( FOXP3 ) and C-X-C Motif Chemokine Receptor 3 ( CXCR3 ) [ 219 , 220 , 221 , 222 , 223 , 224 , 225 ]. Supporting this hypothesis, a study performed on two unrelated families (each one with a pair of male brothers with severe COVID-19) identified two variants in TLR7 : (I) a pLOF variant NM_016562.3 c.2129_2132del, p.(Gln710Argfs*18) in the first family and (II) a missense variant NM_016562.3 c.2383G>T, p.(Val795Phe) in the second family.…”
Section: Discussionmentioning
confidence: 99%