Human Papillomavirus (HPV) can cause benign lesions such as skin warts, condylomata, epidermodysplasia; and malignant lesions, especially invasive cervical cancer. According to the World Health Organization estimators, there are more than 500,000 new cases of invasive cervical cancer annually and more than 250,000 deaths, of which 80% occur in developing countries. HPV types that infect the anogenital region can be classified according to their oncogenic potential into: high-risk and low-risk HPV types. There are descriptions of high-risk HPV types associated with benign lesions, as well as the opposite is true, ie, low-risk HPV types associated to malignant lesions. Until this moment, it is not clear why viruses belonging to the same HPV type cause no or very distinct proliferative responses. Molecular studies have identified HPV variants, confering different risks of progression to invasive cervical cancer, using the URR region. Another study was able to associate the E5 protein to the phenotype. These findings suggest that a single HPV region is not enough to determine the phenotype. However, no study so far has evaluated, in this context, full length viruses. The present study aims to sequence and analyze the complete genome of HPV-16, prototype of high-risk HPVs, and HPV-11, prototype of low-risk HPVs from samples displaying normal cytology, benign and malignant lesions, aiming to identify molecular patterns correlating to the rare phenotypes.
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