GSH and analogs in antiviral therapy

Oxidative stress fuels Trypanosoma cruzi infection in mice

“…The HO-1-mediated increase in bacterial clearance during sepsis has been associated with increased phagocytosis that could potentially mediate the protective effects (25). Antioxidants have been found to reduce pathogen burden in a number of infections (16)(17)(18), while hydrogen peroxide increased Mycobacterium abscessus burden (19), indicating that ROS can be counterproductive in some infections. We showed here that HO-1 induction reduces macrophage parasitism and parasitemia, which correlated positively with oxidative stress and the labile iron pool.…”

“…There are a few exceptions to the rule that ROS are detrimental to pathogen growth: antioxidant administration, as well as deficiency in NOX2, decrease pathogen burden in some viral infections (16)(17)(18), and ROS favor the growth of Mycobacterium abscessus inside macrophages (19). The expression of NRF2 target antioxidant genes is thus expected to weaken defenses against ROS-sensitive pathogens.…”

Redox Remodeling by Dendritic Cells Protects Antigen-Specific T Cells against Oxidative Stress

“…In several chronic infections, in particular HIV infection, there is an imbalance in the redox status of T cells, with ensuing dysfunction and apoptosis in T cell subsets (30)(31)(32). Collectively, these previous studies highlighted that the redox balance of T cells is critical for T cell function and survival and point to the possibility of controlling thiols and, hence, modulating T cell function and survival, by pharmacological intervention (30,32).…”

“…In cancer, ROS produced by myeloid-derived suppressor cells are assumed to inhibit cytotoxic T cell responses (26,27); in contrast, a reduced ROS production in mice with an allelic polymorphism in Ncf1, which encodes a component of the ROSgenerating NADPH oxidase, entails increased T cell thiol expression, dysfunctional elimination of autoreactive T cells, and development of autoimmunity (16,28,29). In several chronic infections, in particular HIV infection, there is an imbalance in the redox status of T cells, with ensuing dysfunction and apoptosis in T cell subsets (30)(31)(32). Collectively, these previous studies highlighted that the redox balance of T cells is critical for T cell function and survival and point to the possibility of controlling thiols and, hence, modulating T cell function and survival, by pharmacological intervention (30,32).…”

Respiratory Viral Infections and Subversion of Cellular Antioxidant Defenses

“…Scavenge OH -free radicals and Inhibited synthesis negative strand RNA and viral replication in vitroand in vivo [72,94] N-Acetyl-L-cysteine (NAC) Inhibited induction of apoptosis and pro-inflammatory cytokines such as IL-6, IL-8 and RANTES [95,96] Glutathione Inhibited induction of apoptosis and viral replication in vitroand in vivo [97,98] infections. Antioxidants reduce oxidative stress by quenching free radicals and help the host to function properly.…”