Journal
AIDS
Volume 21, Issue 6, Pages 755-759Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/QAD.0b013e328012b838
Keywords
HIV-1; endometritis; cervicitis; bacterial vaginosis; shedding; infectivity; Kenya; pelvic inflammatory disease
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Funding
- NICHD NIH HHS [HD40540, 5T32HD40671] Funding Source: Medline
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Objectives: To determine the effects of vaginal, cervical, and endometrial infections on shedding of HIV-1 RNA in the female genital tract. Design: Cross-sectional. Methods: Antiretroviral-naive women from Nairobi, Kenya with CD4 cell counts > 350cells/mu l had plasma and enclocervical wick samples collected for HIV quantification by real-time RNA reverse transcriptase-polymerase chain reaction. Vaginal and cervical Gram stains and endometrial biopsies were obtained. Vaginal Gram stain was used to diagnose bacterial vaginosis and to quantify Lactobacillus levels. Results: Twenty-six of 50 (52%) women had detectable enclocervical HIV-1 RNA with a median endocervical viral load of 1760copies/ml (range: undetectable to 1 030000copies/ml). Women with decreased Lactobacillus had 15.8-fold [95% confidence-interval (CI), 2.0-123] greater enclocervical HIV-1 RNA than women with normal Lactobacillus levels. Women with plasma cell (PC) endometritis [>= 1 PC/ high-power field (hpf)] had a 15.8-fold (95% CI, 2.0-120) higher enclocervical HIV RNA level than women without PC endometritis. Both these associations remained after controlling for plasma viral load. Cervicitis (>= 30 polymorphonuclear leukocytes/hpf), however, was not associated with endocervical HIV-1 RNA shedding (P=0.81). Conclusions: In HIV-1-infected, antiretroviral-naive women without symptoms of pelvic inflammatory disease infection, abnormal vaginal flora and inflammatory cells in the endometrium affected HIV-1 shedding from the lower genital tract. These data suggest that both the upper and lower genital tracts contribute to female HIV-1 genital shedding. (c) 2007 Lippincott Williams & Wilkins.
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