Vaccinating guinea pigs with recombinant glycoprotein D of herpes simplex virus in an efficacious adjuvant formulation elicits protection against vaginal infection.

Guinea pigs were immunized with glycoprotein gD-2t in SAF-m or saline, then challenged with herpes simplex virus, type 2 (HSV-2). Animals given gD-2t in SAF-m had higher anti-gD-2t antibodies, fewer and less severe vaginal lesions, and decreased ganglionic latency compared to animals given gD-2t in saline. Leucocytes from animals vaccinated with gD-2t in SAF-m had greater proliferative responses to gD-2t in vitro than cells from control animals. MHC II-restricted, gD-2t-specific cytotoxic T cells were induced in guinea pigs vaccinated with gD-2t in SAF-m. Thus, immunization of guinea pigs with gD-2t in SAF-m markedly reduced the incidence and severity of primary HSV-2 by eliciting both humoral and cell-mediated responses.

Lack of antiviral activity of ketoconazole alone or in combination with the acyclic nucleoside ganciclovir against a herpes virus type 2 infection in mice.

Ketoconazole and ganciclovir were tested for antiviral activity, each alone and in combination, against a herpes simplex virus type 2 (HSV-2) systemic infection in Swiss-Webster mice. When given once daily for 5 days starting 24 hr after infection, the ED50 for ketoconazole either alone or in combination was greater than 60 mg/kg; for ganciclovir, the ED50 was 7.1 mg/kg alone and 10.8 mg/kg in combination. Thus, ketoconazole did not potentiate or antagonize the antiviral activity of an acyclic nucleoside. Consequently, AIDS patients could perhaps receive ketoconazole and ganciclovir simultaneously for fungal and viral opportunistic infections without interference with their respective efficacies.

Efficacy of interleukin-1 beta against systemic Candida albicans infections in normal and immunosuppressed mice.

Prophylactic treatments with either recombinant human interleukin-1 beta (rHuIL-1 beta) or a muramyl dipeptide analog ([Abu1]MDP) enhanced the resistance of mice to systemic infection with Candida albicans. The optimum treatment regimen in both normal and cyclophosphamide-treated mice was intraperitoneal administration of 100 ng of rHuIL-1 beta or 1.6 mg of [Abu1]MDP per mouse once daily for 3 consecutive days before infection. Neither rHuIL-1 beta nor [Abu1]MDP was efficacious when started after the infection or when given before cyclophosphamide to mice infected subsequently. Continuing to treat after the infection with either drug neither enhanced nor antagonized the efficacy of prophylactic treatments.