Herpes Simplex Virus Type 2-Induced Mortality following Genital Infection Is Blocked by Anti-Tumor Necrosis Factor Alpha Antibody in CXCL10-Deficient Mice
Copyright policy )Herpes Simplex Virus Type 2-Induced Mortality following Genital Infection Is Blocked by Anti-Tumor Necrosis Factor Alpha Antibody in CXCL10-Deficient Mice
ABSTRACTThe role of tumor necrosis factor alpha (TNF-α) was evaluated for CXCL10-deficient (CXCL10−/−) mice which succumbed to genital herpes simplex virus type 2 (HSV-2) infection and possessed elevated levels of virus and TNF-α but not other cytokines in the central nervous system (CNS) and vaginal tissue within the first 7 days following virus exposure. Anti-TNF-α but not control antibody treatment offsets the elevated mortality rate of CXCL10−/−mice, despite increased CNS viral titers. In addition, TNF-α neutralization suppressed recruitment of leukocyte subpopulations into the CNS, which is associated with reduced CCL2 and CXCL9 expression. Collectively, the results implicate TNF-α as the principal mediator of mortality in response to genital HSV-2 infection.
- University of Oklahoma Health Sciences Center United States
- University of Oklahoma Health Sciences Ctr United States
- Department of Microbiology United States
CD4-Positive T-Lymphocytes, Mice, Knockout, Herpes Genitalis, Antineoplastic Agents, Hormonal, Tumor Necrosis Factor-alpha, Herpesvirus 2, Human, Medroxyprogesterone Acetate, CD8-Positive T-Lymphocytes, Chemokine CXCL9, Antibodies, Chemokine CXCL10, Mice, Spinal Cord, Vagina, Animals, Female, Brain Stem
CD4-Positive T-Lymphocytes, Mice, Knockout, Herpes Genitalis, Antineoplastic Agents, Hormonal, Tumor Necrosis Factor-alpha, Herpesvirus 2, Human, Medroxyprogesterone Acetate, CD8-Positive T-Lymphocytes, Chemokine CXCL9, Antibodies, Chemokine CXCL10, Mice, Spinal Cord, Vagina, Animals, Female, Brain Stem
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