HSV-2病毒是生殖器疱疹的主要病原，一旦感染，患者将终身携带这种病毒并周期性地出现生殖器疱疹性损伤，HSV-2感染还会增加HIV-1传播的风险，且目前没有针对HSV-2的有效
疫苗问世。由于HSV-2的高阳性率及与HIV-1共同的传播途径，针对HSV-2的相关研究越来越受到重视。
生殖道黏膜部位不易建立针对HSV-2长期有效的记忆性免疫保护，这成为疱疹病毒疫苗研制的主要瓶颈。胡勤学学科组利用了趋化因子CCL19能够靶向性地趋化和招募
免疫细胞到次级淋巴器官及黏膜组织的特性，将候选免疫原HSV-2 gB蛋白与CCL19 制成嵌合的DNA疫苗。结果发现“gB-CCL19”嵌合疫苗能够在小鼠体内诱导很好的保护作用，从而为设计针对HSV-2或其他性传播病毒的疫苗奠定了基础。
HSV-2 is the major cause of genital herpes, and its infection increases the risk of HIV-1 acquisition and transmission. After initial infection, HSV-2 can establish latency within the nervous system and thus maintains lifelong infection in humans. It has been suggested that HSV-2 can inhibit type I IFN signaling, but the underlying mechanism has yet to be determined. In this study, we demonstrate that productive HSV-2 infection suppresses Sendai virus (SeV) or polyinosinic-polycytidylic acid-induced IFN-β production. We further reveal that US1, an immediate-early protein of HSV-2, contributes to such suppression, showing that US1 inhibits IFN-β promoter activity and IFN-β production at both mRNA and protein levels, whereas US1 knockout significantly impairs such capability in the context of HSV-2 infection. US1 directly interacts with DNA binding domain of IRF-3, and such interaction suppresses the association of nuclear IRF-3 with the IRF-3 responsive domain of IFN-β promoter, resulting in the suppression of IFN-β promoter activation. Additional studies demonstrate that the 217–414 aa domain of US1 is critical for the suppression of IFN-β production. Our results indicate that HSV-2 US1 downmodulates IFN-β production by suppressing the association of IRF-3 with the IRF-3 responsive domain of IFN-β promoter. Our findings highlight the significance of HSV-2 US1 in inhibiting IFN-β production and provide insights into the
molecular mechanism by which HSV-2 evades the host innate immunity, representing an unconventional strategy exploited by a dsDNA virus to interrupt type I IFN signaling pathway.
