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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.
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Together, these results indicate that OASL1-mediated negative regulation of type I IFN production suppresses both innate and adaptive immunity against mucosal HSV-2 infection.
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