Two hundred eight cervical specimens from two groups of subjects, 165 nonpregnant women and 53 pregnant women with cervical intraepithelial neoplasia (CIN) of grades I to III, were positive by PCR analyses for human papillomaviruses (HPVs), adeno-associated virus type 2 (AAV 2), and human cytomegalovirus (HCMV) in 67, 6, and 4.1% of the cases, respectively. The presence of AAV 2 infection was more frequently associated with pregnancy (17 versus 2.4%) and HPV-positive cervices (odds ratio ؍ 6.358) than HCMV was. Increased HPV infection was strongly associated (P < 0.001) with a higher CIN grade, but there is no evidence that AAV 2 and HCMV infections have any impact on CIN development.The causal role of human papillomavirus (HPV) infections in cervical cancer development has been well established in the last 2 decades (2). More than 40 HPV genotypes infect the genital tract; however, only a subset of high-risk HPVs is involved in cervical cancer pathogenesis, most notably HPV type 16 (HPV 16), found in more than 50% of cervical cancer cases worldwide.Latent HPV infection is found in approximately 40% of young women, but only 1% of high-risk HPV-positive cervices (or fewer) will develop cervical cancer (2). Since only a small fraction of HPV-infected women develop cervical cancer, additional risk factors are likely to be important determinants of disease development. These factors could include hormonal factors, other sexually transmitted infections, tobacco smoking, and dietary factors (4).It is still unclear whether other infectious agents contribute to increased cervical cancer risk. A history of multiple genital infections is more common in women with cervical cancer (8), suggesting that these agents might increase the risk of developing cancer. However, the possibility that their presence may be an indicator of sexual activity and hence a surrogate marker of oncogenic HPV infection cannot be excluded.Most adults (80 to 90%) are infected with adeno-associated virus (AAV) (9), which is commonly carried in the genital region (11). AAV is a human helper virus-dependent parvovirus with the ability to suppress the oncogenic phenotype of a variety of viruses and oncogenes. From in vitro studies, AAV has been shown to prevent the replication of HPVs and therefore may protect infected patients from cervical intraepithelial neoplasia (CIN) (13). However, in vivo studies of women with cervical HPV infection or CIN gave inconsistent results regarding the role of AAV in cervical carcinogenesis (16,20).Human cytomegalovirus (HCMV), a widespread human herpesvirus, has been shown to induce cervical neoplasia in mice (12), to morphologically transform human cells in culture (15), and to cause persistent infections of the genitourinary tracts of women (6). However, HCMV DNA is not detected in most transformants and the mechanism by which HCMV might contribute to oncogenesis is still unclear.The aim of this retrospective study was to determine whether infection with AAV and/or HCMV influences the already established oncogenic...
The association between certain human papillomaviruses (HPV) and cervical intraepithelial neoplasia (CIN) is well documented, but still unknown among Croatian women. In 1995, women between the age of 17 and 64 with cytomorphologically abnormal smears (CIN I-IV) were tested for the presence of HPV. Consensus and specific primers were used in the polymerase chain reaction (PCR) to detect the most common types: 6, 11, 16, 18, 31 and 33, as well as the unknown-risk HPV types (HPV X). Out of 379 specimens, 163 (43%) contained one or more HPV types. Coinfection with different HPV types in the same sample was observed in 16 cases. Beside low-risk HPV 6/11 (25.8%) the most frequently observed types were high-risk HPV types 16 (20.2%) and 31 (17.8%). Globally, the HPV positivity rate declines with age. The presence of HPV DNA significantly increased from 35.5 to 61.1% along with the severity of the cervical intraepithelial neoplasia (CIN I-IV). HPV type 6/11 was strongly associated with CIN I (33.8%), HPV type 31 with CIN II (22.9%), and HPV type 16 with CIN III (50%).
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