Furthermore, whether OASL1 also regulates type III IFNs has not been investigated.In the present study, we show that Oasl1 BM cells after in vitro stimulation with HSV-2, type III IFN remained high in vaginal washes until later time points after intravaginal HSV-2 infection.In addition to genital ulcers, HSV-2 infection can cause severe and frequently fatal symptoms, and is considered to be a major risk factor for other STIs such as human immunodeficiency virus type 1 (HIV-1).Thus, understanding host immune responses against HSV-2 infection may provide clues for the cure and prevention of this debilitating disease.Oasl1 mice exhibited better survival rates than wild type (WT) mice following intravaginal HSV-2 infection, and suppressed virus replication more efficiently despite comparable recruitment of effector immune cells. Collectively, these results demonstrate that OASL1 deficiency promotes antiviral immunity against local mucosal viral infection and suggest that OASL1 could be a therapeutic target for treatment of HSV-2 infection of the genital mucosa.Genital herpes is one of the most common sexually transmitted infections (STIs) worldwide.
To this end, we investigated the role of OASL1 during mucosal HSV-2 infection of the genital tract.
Data are representative of three independent experiments.
(d) Expression of ISGs in vaginal tissue of uninfected Oasl1Unlike systemic viral infection, both hematopoietic and stromal compartments take part in innate immune responses after mucosal HSV-2 infection.
Thus, to determine whether OASL1 also regulates type III IFN, we measured the level of IFN-λ in vaginal washes after mucosal HSV-2 infection.
Unlike IFN-α, the level of IFN-λ at the infection site in Oasl1 BM cells after stimulation with HSV-2 (Fig. In addition, similar amounts of IL-12p40, a pro-inflammatory cytokine important for the differentiation of Th1 cells, were produced by infected control and Oasl1 mice were stimulated with TK- HSV-2 at the indicated MOIs for 18 h.