Genital tract infections, including vulvovaginal candidiasis (VVC) and bacterial vaginosis (BV), have emerged as potential modulators of persistent human papillomavirus (HPV) infections causing cervical cytological abnormalities (CA) and cervical cancer. This study aimed to investigate whether VVC or BV had an additional effect on HPV infection and thus caused such abnormalities. ThinPrep cytological tests were used to detect CA, VVC, and BV in 14,679 women. Cytological abnormalities included atypical squamous cells of undetermined significance (ASC-US), low-grade squamous intraepithelial lesions (LSIL), high-grade squamous intraepithelial lesions (HSIL), atypical squamous cells-cannot exclude HSIL (ASC-H), and squamous cell carcinoma (SCC). Logistic regression Model 1 (univariate regression) and Model 2 (multivariate logistic regression analysis adjusted for age combined with HPV infection) were used to analyze the association between BV and CA, or VVC and CA, alone or in the presence of HPV infection. BV infection rates were found to be significantly higher in the cytology-negative group among all participants and those with HPV infection (p=0.003, p<0.001, respectively). Analyses using Model 1 and Model 2 both pointed to BV as a protective factor against CA for all participants (OR=0.36, 0.17, respectively, p<0.05) and for HPV-infected participants (OR=0.17, 0.16, respectively, p<0.05). Neither VVC nor VVC + HPV was significantly associated with the incidence of CA based on Model 1 (OR=0.94, 0.71, respectively, p>0.05) and Model 2 (OR=0.91, 0.74, respectively, p>0.05). Furthermore, neither VVC nor BV increased the incidence of CA regardless of HPV infection status, while BV might possibly prevent CA in women co-infected by HPV.
