Susceptibility of human female primary genital epithelial cells to herpes simplex virus, type-2 and the effect of TLR3 ligand and sex hormones on infection.

Genital epithelial cells (ECs) are the first line of defense that sexually transmitted viruses encounter. The mechanism of viral pathogenesis in these cells is not well understood. Here, we show that a primary cell culture model from human reproductive tract tissues can be used as a novel ex vivo model in examining the interaction of herpes simplex virus, type 2 (HSV-2), with female genital mucosa.

Expression of Toll-like receptors in murine vaginal epithelium is affected by the estrous cycle and stromal cells.

Vaginal epithelium is regulated by female sex hormones and serves as the first line of innate immune defense against sexually transmitted infections (STIs). This occurs in part through recognition of pathogens via Toll-like receptors (TLRs); however, the expression and role of TLRs in reproductive tract immunity are poorly understood. Here, we have compared the effect of the estrous cycle and treatment with DepoProvera (Depo) on TLR mRNA expression in whole mouse vaginal tissue, vaginal epithelium isolated using laser capture microdissection (LCM) and in primary vaginal epithelial cells (ECs) grown in vitro.

Differential responses of murine vaginal and uterine epithelial cells prior to and following herpes simplex virus type 2 (HSV-2) infection.

Problem: This study was undertaken to evaluate the susceptibility of upper and lower reproductive tract epithelial cells (ECs) to herpes simplex virus type 2 (HSV-2) infection and examine their cytokine secretion patterns prior to and following infection.

Method Of Study: Primary EC cultures, grown from murine vaginal and uterine tissue, were inoculated with HSV-2. Viral shedding was measured in apical and basolateral compartments.

Estradiol regulates susceptibility following primary exposure to genital herpes simplex virus type 2, while progesterone induces inflammation.

We report here that sex hormones modulate susceptibility to a sexually transmitted viral agent, herpes simplex virus type 2 (HSV-2), in a mouse model. Ovariectomized mice were administered either saline (control), estradiol (E(2)), progesterone (P(4)), or a combination of both estradiol and progesterone (E+P) and infected intravaginally with HSV-2. With an inoculation dose of 10(5) PFU, the saline- and P(4)-treated mice were found to be highly susceptible to genital HSV-2 infection.