Persistence of high-risk (HR-) human papillomavirus (HPV) infection of the uterine cervix increases the risk of cervical cancer.
Infection with and persistence of high-risk human papillomavirus (HR HPV) are the strongest risk factors for cervical cancer.
Patients with positive screening results and persistence of high-risk human papillomavirus (HPV) infection represent the population at the highest risk for developing cervical cancer.
The short-time persistence of high-risk HPV infection in this age group was about 60%.
Studies showed that type-specific persistence of high-risk human papillomavirus (HPV) infection contributed significantly to cervical carcinogenesis [ 5- 7].
Studies have shown that type-specific persistence of high-risk human papillomavirus (HPV) infection contributed significantly to cervical carcinogenesis.
The persistence of high-risk HPV types in the transformation zone of the cervix ultimately leads to malignant changes in the cervix [ 1, 9, 18].
The increased prevalence of high grade cervical lesions and cervical cancer in immunocompromised patients, such as AIDS patients and transplant recipients, indicates that persistence of high-risk HPV and consequently HPV-mediated carcinogenesis is related to compromised immunosurveillance (IARC, 1995; Petry et al, 1996; Sun et al, 1997).
Future studies looking at the mechanisms of bacterial persistence in high risk groups such as Indigenous Australians would be important in understanding these disease processes and to design more effective treatment and prevention.
The persistence of high-oncogenic risk subtypes has been demonstrated to be a necessary but not sufficient cause of cervical cancer [ 3]; the principal cancer of women in the developing world and second commonest female cancer worldwide [ 4, 5] (~510,000 cases with 288,000 deaths annually) [ 6].
This may have been related to the persistence of higher frequency of high-risk sexual practices in this group, thus suggesting that seeking PEP might be a predictor of HIV infection.
