Multiple factors affect the rate of genital human immunodeficiency virus (HIV) shedding, which subsequently affects vertical transmission and sexual acquisition of HIV. Local genital factors (e.g., genital ulcer disease, bacterial vaginosis, Trichomonas vaginalis) have been shown to increase the risk for sexual transmission of HIV. In one study, women with vulvovaginal candidiasis had increased presence of proviral HIV-1 DNA. In another study, women with vaginal Candida colonization or infection had a higher prevalence of cell-free HIV-1 RNA in cervicovaginal secretions compared with control patients who had negative cultures. Although a link between vaginal infections and HIV transmission has not been established, the factors that influence HIV shedding and replicative life cycle may be important in prevention programs. Spinillo and colleagues evaluated how symptomatic vulvovaginal candidiasis affects HIV-1 shedding in cervicovaginal secretions in women with HIV-1 infection.
The prospective, observational, case-control study included women with known HIV-1 infections and symptomatic vulvovaginal candidiasis. The control group included patients who were seropositive for HIV and negative for vulvovaginal infections. Paired blood and cervicovaginal lavage samples were collected from women in both groups. The blood samples were used to assess the CD4+ lymphocyte cell count and quantifying HIV-1 RNA in plasma. The cervicovaginal samples were used in the quantitative evaluation of proviral HIV-1 DNA, HIV-1 RNA transcripts, and cell-free HIV-1 RNA. Logistic regression analysis was used to evaluate the influence of vulvovaginal candidiasis on the HIV-1 load in cervicovaginal secretions.
Final analysis included 66 patients who were seropositive for HIV with vulvovaginal candidiasis and 249 in the control group. The amount of HIV-1 RNA in plasma was significantly correlated with the cervicovaginal secretion load of HIV-1 DNA, HIV-1 RNA transcripts, and cell-free HIV-1 RNA. Approximately 26 percent of patients who tested negative for HIV-1 RNA in the plasma had HIV-DNA in their cervicovaginal secretions. The presence of vulvovaginal candidiasis was significantly associated with increased loads of cell-free HIV-1 RNA and HIV-1 transcripts.
The authors conclude that the presence of vulvovaginal candidiasis is associated with an increase in the number of copies of cell-associated and cell-free HIV-1 RNA in women who are seropositive for HIV. They add that treatment and adequate prophylaxis of vulvovaginal candidiasis in women with HIV is important in reducing the risk for HIV transmission.