HPV is a double stranded DNA tumor virus that is responsible for causing warts.  Serotypes of this virus exist that have a greater tropism toward the tissues of the anogenital region.  Of these serotypes, several have been identified that are associated with varying levels of risk for development of cancer.  The familiar serotypes that are associated with increased risk of cervical and anal cancer are 16 and 18.  Other serotypes have been identified as carrying an intermediate oncogenic risk; these include serotypes 31, 33, 35, 45, 51, 52, and 56.  The designation of “intermediate risk” may be artifactual secondary to the low incidence of these strains in the population [4].  In one study, PCR of anal cancers revealed that 84% of these tumors were positive for HPV-16 [8].
            The mechanism of oncogenesis is felt to be related to two viral proteins E7 and E6 that respectively bind to host tumor suppressor gene products Rb and p53 leading to a disturbance in the regulation of DNA replication, repair, and cellular growth.  The integration of the HPV genome into host DNA has been found in anogenital cancers.   This genomic integration allows transcription of  the E6 and E7 proteins with the subsequent  enhancement of HPV’s oncogenic potential [4].   HIV infection may also enhance the carcinogenic effect of HPV.  There is some evidence that the HIV tat protein may augment the production of E6 and E7 [5].   Field effect may also participate in the pathogenesis of these cancers with other extrinsic carcinogens, such as those found in tobacco, potentiating the already significant effect of HPV [6]. 
            HPV-associated histological changes found in cervical squamous intraepithelial lesions (CSIL) and anal squamous intraepithelial lesions (ASIL) are felt to be analogous pre-cancerous lesions.  Though the natural course of ASIL to anal cancer is not definitive because of the lack of studies following untreated ASIL, the circumstantial evidence that these lesions are pre-cancerous is compelling [7].