Abstract
Type I interferon (IFN-I) plays a critical role in the antiviral immune response. However, viruses have developed different strategies to suppress the production of IFN-I for its own escape and amplification. Therefore, promoting the production of IFN-I is an effective strategy against virus infection. Gastrodin (GTD), a phenolic glucoside extracted from Gastrodia elata Blume, has been reported to play a protective role in some central nervous system -related diseases and is beneficial for the recovery of diseases by inhibiting inflammation. However, the effect of GTD on virus infection is largely unknown. Here we found GTD treatment increased the survival rate of mice infected with vesicular stomatitis virus (VSV) or herpes simplex virus-1 (HSV-1). The production of IFN-I was increased in GTD-treated mice or macrophages compared to the control group, during virus infection. Furthermore, the activation of interferon regulatory factor 3 (IRF3) was promoted by GTD in macrophages upon VSV and HSV-1 infection. Our results demonstrated that GTD could inhibit the VSV and HSV-1 infection by promoting the production of IFN-I in macrophages and might provide an effective strategy against virus infection.
Highlights
Innate immunity is the first line of defense against virus infection (Corbett et al, 2020; Kucharski and Nilles, 2020; Wandernoth et al, 2020)
Our results demonstrated that GTD could inhibit the vesicular stomatitis virus (VSV) and herpes simplex virus-1 (HSV-1) infection by promoting the production of IFN-I in macrophages and might provide an effective strategy against virus infection
There were lower HSV-1 titers and HSV-1 gDNA copies in the brain of mice with GTD treatment (Figures 1F,G). These findings implied that GTD inhibits RNA virus and DNA virus infection in vivo
Summary
Innate immunity is the first line of defense against virus infection (Corbett et al, 2020; Kucharski and Nilles, 2020; Wandernoth et al, 2020). Innate immune cells such as macrophages and dendritic cells are activated in response to virus infection, which depending on the detection of pathogen-associated molecular patterns (PAMPs) by germline-encoded pattern-recognition receptors (PRRs), including Toll-like receptors (TLRs), Retinoic acid-inducible gene I (RIG-I)-like receptors (RLRS), Nod-like receptors and DNA sensors such as cGAS, IFI16, and DDX41 (Oth et al, 2016; Eppensteiner et al, 2019). The PRRs recruit down-stream adaptors, including TRIF, MAVS and STING, which activate the down-stream kinases TBK1 and IKKε, leading to the activation of nuclear factor-kB and interferon (IFN) regulatory transcription factor (IRF)-3/7 and induction of the production of type I IFN (IFN-I) and proinflammatory cytokines (Chen et al, 2013; Chen et al, 2016; Gao et al, 2018; Liu et al, 2019).
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