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Objective: The purpose of this study was to evaluate the influence of symptomatic vulvovaginal candidiasis on the shedding of HIV- 1 in cervicovaginal secretions of HIV- 1- infected women. Study design: We obtained paired blood and cervicovaginal lavage samples from 66 HIV- infected women with symptomatic vulvovaginal candidiasis, and 249 HIV- infected control patients without genital infection. HIV- 1 RNA in plasma, proviral HIV- 1 DNA, HIV- 1 RNA transcripts, and cell- free HIV- 1 RNA in cervicovaginal secretions were quantitatively evaluated by competitive polymerase chain reaction (cPCR) and reverse transcriptase PCR (cRT- PCR). We used logistic regression on ordered data to assess the influence of vulvovaginal candidiasis on the HIV- 1 load in cervicovaginal secretions adjusting for potential confounders. Results: Overall, the amount of HIV- 1 RNA in plasma was significantly correlated with HIV- 1 DNA (Spearman rank 0.153 ± 0.059, P =. 006), HIV- 1 RNA transcripts (Spearman rank 0.169 ± 0.058, P =. 003), and cell free HIV- 1 RNA (Spearman rank 0.185 ± 0.059, P =. 001) load in cervicovaginal secretion. Forty- eight out of 182 (26.4% ) patients who tested negative for HIV- 1 RNA in plasma were positive for HIV- DNA in their cervicovaginal secretions. In logistic regression analysis vulvovaginal candidiasis was significantly associated with increasing loads of HIV- 1 RNA transcripts (Odds ratio [OR] 1.97, 95% CI 1.09- 3.57, P =. 025) and cell free HIV- 1 RNA (OR 2.03, 95% CI 1.10- 3.73, P =. 02) in cervicovaginal secretions. Conclusion: In HIV- infected women, vulvovaginal candidiasis is associated with an increased number of copies of cell- associated and cellfree HIV- 1 RNA in cervicovaginal secretions.
Objective: The purpose of this study was to evaluate the influence of symptomatic vulvovaginal candidiasis on the shedding of HIV-1 in cervicovaginal secretions of HIV- 1-infected women. Study design: We obtained paired blood and cervicovaginal lavage samples from 66 HIV- infected women with symptomatic vulvovaginal candidiasis, and 249 HIV-infected control patients without genital infection. HIV-1 RNA in plasma, proviral HIV-1 DNA, HIV-1 RNA transcripts, and cell-free HIV- 1 RNA in cervicovaginal secretions were quantitatively evaluated by competitive polymerase chain reaction (cPCR) and reverse transcriptase PCR (cRT-PCR). We used logistic regression on ordered data to assess the influence of vulvovaginal candidiasis on the HIV-1 load in cervicovaginal secretions adjusting for potential confounders. Results: Overall, the amount of HIV-1 RNA in plasma was significantly correlated with HIV-1 DNA (Spearman rank 0.153 ± 0.059, P = 0.006), HIV-1 RNA transcripts 0.169 ± 0.058, P =. 003), and cell free HIV-1 RNA (Spearman rank 0.185 ± 0.059, P = .001) load in cervicovaginal secretion. Forty- eight out of 182 (26.4%) patients who tested negative for HIV - 1 RNA in plasma were positive for HIV-DNA in their cervicovaginal secretions. In logistic regression analysis vulvovaginal candidiasis was significantly associated with increasing loads of HIV-1 RNA transcripts (Odds ratio [OR] 1.97, 95% CI 1.09-3.57, P 025) and cell free HIV-1 RNA (OR 2.03, 95% CI 1.10-3.73, P = .02) in cervicovaginal secretions. Conclusion: In HIV-infected women, vulvovaginal candidiasis is associated with an increased number of copies of cell-associated and cellfree HIV-1 RNA in cervicovaginal secretions.