heme oxygenase-1 agonist CoPP suppresses influenza virus replication through IRF3-mediated generation of IFN-α/β

Nutraceuticals have potential for boosting the type 1 interferon response to RNA viruses including influenza and coronavirus

“…5 Furthermore, HO-1 induction is reported to potentiate the type 1 interferon response to influenza virus. 6 Phase 2inductive nutraceuticalssuch as ferulic acid, lipoic acid, or sulforaphaneare known to promote induction of HO-1, and hence may have some utility for boosting type 1 interferon response. [7][8][9] The ability of sodium ferulate to activate TLR7, stimulate type 1 interferon production, and enhance survival in influenza A-infected mice, might be secondary to HO-1 induction, and possibly reflects an additional effect of ferulate per se (as TLR9 was also found to be activated).…”

Heme oxygenase-1 (HO-1) cytoprotective pathway: A potential treatment strategy against coronavirus disease 2019 (COVID-19)-induced cytokine storm syndrome

“…A recent study has highlighted the antiviral effect of HO-1 against influenza viruses. Indeed, authors showed that cobalt protoporphyrin (CoPP), a potent HO-1 inducer similar to hemin, inhibits influenza A virus replication through HO-1 interaction with IRF3 and subsequent expression of IFNα/β [26] . A same mechanism was found in human respiratory syncytial virus infection with attenuation of viral replication and lung inflammation upon HO-1 induction and expression of IFNα/β in the infected lung [27] .…”

“…A same mechanism was found in human respiratory syncytial virus infection with attenuation of viral replication and lung inflammation upon HO-1 induction and expression of IFNα/β in the infected lung [27] . Of note, HO-1-mediated type I IFN response may control numerous of other viral infections, such as hepatitis B/C virus, Ebola virus, and human immunodeficiency virus by inhibiting virus replication [26] . By inference, these data suggest that hemin-induced HO-1may be also used to overcome the outbreak of COVID-19 by inhibiting SARS-CoV-2 replication.…”

Downregulation of SOCS gene expression can inhibit the formation of acute and persistent BDV infections

“…11 Hepatitis C virus (HCV), human parainfluenza virus type 2, measles virus, influenza A virus, hepatitis B virus (HBV) and other viruses inhibit the IFN signalling pathway through various channels, escape the immune response or establish a persistent infection state. [25][26][27][28][29] Studies have shown that in a persistent HPV infection, the targeted inhibition of SOCS1 can promote type I IFN to exert antiviral functions 30 and that small molecule inhibitors of ubiquitin-specific proteinase 7 can inhibit SOCS1 expression and enhance the antiviral effect of type I IFN. 31 It has also been shown that the targeted inhibition of the SOCS1/NF-KB pathway promotes type I IFN production and can also limit human cytomegalovirus replication.…”