The complexity of contraceptives: understanding their impact on genital immune cells and vaginal microbiota

SL Achilles, SL Hillier - Aids, 2013 - journals.lww.com
Aids, 2013journals.lww.com
The same populations of women at risk for sexual acquisition of HIVare also at risk for
pregnancy; many of these women use contraception. Combating the spread of HIV is a
major global goal [1] ideally achievable with development of highly effective dual protection
methods that prevent both sexual acquisition of HIVand unwanted pregnancy. Currently,
emerging evidence [2] suggests that some commonly used contraceptives may increase risk
of sexual HIVacquisition and transmission. There are several biologically plausible …
The same populations of women at risk for sexual acquisition of HIVare also at risk for pregnancy; many of these women use contraception. Combating the spread of HIV is a major global goal [1] ideally achievable with development of highly effective dual protection methods that prevent both sexual acquisition of HIVand unwanted pregnancy. Currently, emerging evidence [2] suggests that some commonly used contraceptives may increase risk of sexual HIVacquisition and transmission. There are several biologically plausible mechanisms by which hormonal contraceptives could increase HIV risk including disrupting epithelial barriers (thinning of the epithelium or altering epithelial integrity), causing changes in inflammatory responses that could in turn enhance HIV replication locally [3], or altering the vaginal microbiota which itself effects local immunity and genital inflammation. The objective of this manuscript is to review the evidence linking contraceptives to genital tract changes and to identify research gaps to be addressed with future studies.
The anatomic, immune, and microbiological milieu of the female genital tract may be important determinants of both HIV acquisition and sexual transmission [4]. The likelihood of HIV acquisition when a susceptible individual is sexually exposed is driven by several factors, including viral load of the transmitting sexual partner [5], however, host factors are also important in acquisition risk. One potentially important host factor in HIV acquisition risk is the number of accessible cellular targets available for viral entry, a necessary step prior to systemic dissemination [3]. Genital tract immune cells are common portals of entry for HIV [3, 6] yet little is
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