Human α-interferons (IFN-αs) made in bacteria were examined for antiviral activity against herpes simplex virus type 2 (HSV-2) infections of mouse L-cells , and acute cervicovaginal and lethal systemic HSV-2 infections of BALB/c mice. The recombinant DNA-derived hybrid interferon IFN-αAD(Bgl) showed pronounced antiviral activity , exceeding the activity of either of the parental subtypes IFN-αA and IFN-αD and that of the other hybrids IFN-αAD(Pvu). A combination of topical and systemic treatments with IFN-αA and IFN-αAD(Bgl) failed to protect mice from subsequent challenge with an acute cervicovaginal infection of HSV-2. Protection from lethal systemic HSV-2 infection in mice was observed when IFN-αAD(Bgl) and IFN-αAD(Pvu) were administered systemically, whereas IFN-αA failed to confer protection. These results suggest that for protection against infection with HSV-2, the routes of introduction of the virus and of the interferon influence the host response to interferon therapy.


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