Abstract

Worldwide, 18.5 million women are infected with the human immunodeficiency virus (HIV-1). At least 80% of these HIV infections have occurred as a result of sexual intercourse with an infected male partner. This review focuses on how HIV-1 enters the human female reproductive tract, and how oestrogen or progesterone, by altering the cervicovaginal epithelium, might change a woman's susceptibility to HIV infection. Experiments on hysterectomised Rhesus monkeys suggest that the vagina, rather than the cervix or uterus, is the main site of viral entry. If ovariectomised monkeys are given systemic oestrogen treatment, this makes them completely resistant to infection by intravaginally administered simian immunodeficiency virus (SIV), whereas progesterone-treated animals, like the untreated controls, are extremely susceptible. Some studies have also shown that women on systemic long-acting gestagen-only contraceptives have a thinner vaginal epithelium and hence might be more susceptible to HIV infection; this is certainly true of post-menopausal women. The beneficial effects of oestrogen are thought to be due to increased thickness and cornification of the cervicovaginal epithelium, which prevents the virus from coming into contact with the target Langerhans cells (LCs). Topical vaginal oestrogen treatment is widely used as a safe and effective way of thickening and keratinising the vaginal epithelium in post-menopausal women. Perhaps this could be an exciting new way of protecting women from HIV infection.

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