The innate immune responses triggering production of type 1 interferons and inflammatory cytokines constitute a nonspecific innate resistance that eliminates invading pathogens including viruses. The acti- vation of i...The innate immune responses triggering production of type 1 interferons and inflammatory cytokines constitute a nonspecific innate resistance that eliminates invading pathogens including viruses. The acti- vation of innate immune signaling through pattern recognition receptors （PRRs） is by sensing pathogen- associated molecular patterns derived from viruses. According to their distribution within cells, PRRs are classified into three types of receptors： membrane, cytoplasmic, and nuclear. Kaposi＇s sarcoma- associated herpesvirus （I（SHV）, a large DNA virus, replicates in the nucleus. Its genome is protected by capsid proteins during transport in the cytosol. Multiple PRRs are involved in KSHV recognition. To suc- cessfully establish latent infection, KSHV has evolved to manipulate different aspects of the host antiviral innate immune responses. This review presents recent advances in our understanding about the activation of the innate immune signaling in response to infection of KSHV. It also reviews the evasion strate- gies used by KSHV to subvert host innate immune detection for establishing a persistent infection.展开更多
基金supported by the National Key R&D Program of China (2016YFA0502100)the Natural Science Foundation for Distinguished Young Scholars (81425017)the National Institutes of Health (7R01AI116442) to K.L.
文摘The innate immune responses triggering production of type 1 interferons and inflammatory cytokines constitute a nonspecific innate resistance that eliminates invading pathogens including viruses. The acti- vation of innate immune signaling through pattern recognition receptors （PRRs） is by sensing pathogen- associated molecular patterns derived from viruses. According to their distribution within cells, PRRs are classified into three types of receptors： membrane, cytoplasmic, and nuclear. Kaposi＇s sarcoma- associated herpesvirus （I（SHV）, a large DNA virus, replicates in the nucleus. Its genome is protected by capsid proteins during transport in the cytosol. Multiple PRRs are involved in KSHV recognition. To suc- cessfully establish latent infection, KSHV has evolved to manipulate different aspects of the host antiviral innate immune responses. This review presents recent advances in our understanding about the activation of the innate immune signaling in response to infection of KSHV. It also reviews the evasion strate- gies used by KSHV to subvert host innate immune detection for establishing a persistent infection.
