OASL1 deficiency promotes antiviral protection against genital herpes simplex virus type 2 infection by enhancing type I interferon production

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Type I interferon (IFN) interferes with virus replication, promotes antiviral responses, and controls innate and adaptive immune responses to certain viruses. Recently, we reported that 2'-5' oligoadenylate synthetase-like 1 (OASL1) negatively regulates type I IFN production by inhibiting the translation of the type I IFN-regulating master transcription factor, IRF7. Notably, while OASL1-deficient mice induce robust production of type I IFN and are resistant to systemic viral infection, the effects of OASL1 during localized viral infection has not been studied. To this end, we investigated the role of OASL1 during mucosal HSV-2 infection of the genital tract. 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. Moreover, Ly6C(high) monocytes, and not pDCs or other cell types, displayed enhanced production of type I IFNs in Oasl1(-/-) mice in response to HSV-2 infection. Furthermore, cytotoxic T cell responses including IFN-gamma production were accelerated in Oasl1(-/-) mice after mucosal HSV-2 infection. 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
Publisher
NATURE PUBLISHING GROUP
Issue Date
2016-05
Language
English
Article Type
Article
Keywords

PLASMACYTOID DENDRITIC CELLS; IMMUNE-RESPONSES; IFN-LAMBDA; INDUCTION; MUCOSAL; ACTIVATION; FAMILY; TISSUE; IRF-7; HSV-2

Citation

SCIENTIFIC REPORTS, v.196

ISSN
2045-2322
DOI
10.1038/srep19089
URI
http://hdl.handle.net/10203/207710
Appears in Collection
MSE-Journal Papers(저널논문)
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