Adeno-associated virus infection and cervical neoplasia: is there a protective role against human papillomavirus-related carcinogenesis?

The aim of this study was to investigate whether adeno-associated virus (AAV) infection can be associated with a reduced risk for human papillomavirus (HPV)-related cervical neoplasia. The study was a prospective descriptive analysis of the prevalence of AAV and HPV DNA sequences in women with and without neoplastic cervical lesions. The study population consisted of 373 women aged 19-65 years old who attended the outpatient colposcopy clinic of a tertiary university center. Cytologic and colposcopic examination, as well as AAV-DNA and HPV-DNA detection and typing were performed in all individuals; biopsies (histological verification) and treatment were performed as appropriate. Women with normal Papanicolaou smear test and normal colposcopic findings served as the control group (n = 280). Those with histologically proven cervical pathology were categorized into three groups: (a) women with grade 1 cervical intraepithelial neoplasia (CIN 1) (n=31), (b) women with grades 2 and 3 cervical intraepithelial neoplasia (CIN 2, 3) (n=45), and (c) women with invasive cervical cancer (n=17). AAV infection was confirmed in 63 (16.80%) women. AAV detection was not statistically different between HPV (-) and HPV (+) controls (P=0.06). In the disease groups, however, the prevalence of AAV was statistically significantly lower in the HPV (+) relative to the HPV (-) patients (P=0.0009, P=0.00001, and P=0.0225, for women with low-grade cervical lesions, for women with high-grade cervical lesions, and for women with cervical cancer, respectively). No difference in the prevalence of AAV DNA between HPV-positive and HPV-negative unaffected (control) women is observed. Nevertheless, our results indicate that HPV-infected individuals are less likely to develop cervical neoplasia if AAV is present, and that AAV probably demonstrates a protective role against the pathogenic consequences of HPV infection.