concanavalin-a and Herpes-Genitalis

Microbicide candidates were selected that have demonstrated activity against sperm or sexually transmitted disease pathogens in vitro, and the efficacy of these agents for preventing vaginal transmission of genital herpes infection was evaluated in the progestin-treated mouse. Each agent was delivered to the vaginas of mice approximately 20 sec prior to delivering a highly infectious herpes simplex virus-2 inoculum. The following agents provided significant protection: anti-HSV monoclonal antibodies III-174 and HSV8, modified bovine beta-lactoglobulin (beta-69), carrageenan, concanavalin A, chlorhexidine, dextran sulfate (average molecular weight 8,000 and 500,000), fucoidan, neem, nonoxynol-9, polystyrene sulfonate, and povidone-iodine. Two agents, gramicidin and heparan sulfate, though highly effective in vitro, were not protective in vivo at the doses tested.

Topics: Animals; Anti-Infective Agents; Antibodies, Monoclonal; Antiviral Agents; Carrageenan; Chlorhexidine; Concanavalin A; Female; Herpes Genitalis; Herpesvirus 2, Human; Lactoglobulins; Mice; Mice, Inbred C57BL; Nonoxynol; Polysaccharides; Polystyrenes; Povidone-Iodine; Vagina

Interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha production and lymphocyte proliferation in response to herpes simplex virus (HSV) antigen were assessed in 13 neonates and 3 parturient women with primary HSV infection. In comparison with 9 nonparturient adults, the neonates and parturient women showed significantly (P less than .01) diminished HSV antigen-stimulated lymphocyte proliferation and IFN-gamma production in the first 3-6 weeks after onset of infection. TNF alpha production did not differ significantly among HSV-infected groups. The impairment in neonatal cellular immunity was due, at least in part, to a specific deficit in response to HSV antigen. Lymphocyte proliferation and TNF alpha production in response to the mitogen concanavalin A (ConA) were comparable in adults and infants, but ConA-stimulated IFN-gamma production in infants was diminished throughout the study period. In contrast, HSV antigen-stimulated IFN-gamma production was comparable in infants and adults after 6 weeks. Not all patients with diminished cellular immune responses to HSV antigen manifested severe clinical disease. Nevertheless, patients with significant clinical morbidity had diminished cellular immune responses to HSV antigen. These results suggest that delayed acquisition of antigen-specific cellular immunity in primary HSV infection predisposes to more severe clinical disease.

Topics: Antibodies, Viral; Antigens, Viral; Blotting, Western; Concanavalin A; Female; Herpes Genitalis; Herpes Simplex; Humans; Immunity, Cellular; Immunity, Maternally-Acquired; Infant, Newborn; Interferon-gamma; Lymphocyte Activation; Pregnancy; Puerperal Infection; Simplexvirus; Time Factors; Tumor Necrosis Factor-alpha

Numerous clinical situations, demonstrated to be associated with reactivation of herpes simplex virus infections, have also been shown to produce increases in local levels of prostaglandins. The current study was initiated to determine if prostaglandins play a role in the immune response and control of herpes simplex virus infections. Lymphocytes from volunteers were stimulated with concanavalin A, herpes simplex virus 1, or herpes simplex virus 2 in the presence of prostaglandin E2 or ibuprofen, and the lymphocytes served as their own controls. The data suggest a statistically significant suppression in nonspecific T cell mitogen stimulation (concanavalin A), as well as specific herpes simplex virus 1 and 2 stimulations as measured by tritiated thymidine uptake by lymphocytes when stimulated in the presence of prostaglandin E2. Ibuprofen did not alter the proliferative response to concanavalin A, herpes simplex virus 1, or herpes simplex virus 2 stimulation. This report examines the involvement of prostaglandins in herpesvirus infection such as the suppression of T cell function, allowing for a clinical recurrence. The usefulness of nonsteroidal antiinflammatory agents in the therapy of herpes simplex virus infections is also discussed.

Topics: Adolescent; Adult; Cell Transformation, Viral; Concanavalin A; Dinoprostone; Female; Herpes Genitalis; Herpes Simplex; Humans; Ibuprofen; Leukocyte Count; Lymphocyte Activation; Male; Middle Aged; Prostaglandins E; Stomatitis, Herpetic; T-Lymphocytes; Time Factors