cervical cancer is the second most prevalent cancer worldwide and is the second leading cause of cancer deaths in women. persistent infection with high-risk human papillomaviruses (hpvs) types are the causative agents of cervical cancer, since 99% of tumors are positive for hpv dna, hpv is a necessary cause of invasive cervical cancer worldwide. one of the key events of hpv-induced carcinogenesis is the integration of the hpv genome into a host chromosome, related with precancerous lesions progression. integration follows a more specific pattern with respect to the hpv genome, expression of the viral e6 and e7 genes is consistently maintained, whereas other positions of the viral dna are deleted or their expression is disturbed, like e2 gene. loss of expression of the hpv e2 transcriptional repressor is significant and may be critical for malignant progression, as it may result in increased hpv e6 and e7 expression. the hpv e6 and e7 oncoproteins inactivate the p53 and prb tumor suppressors; expression of high-risk hpv e6/e7 oncogenes provides a subset of the minimally required carcinogenic hits for full transformation of human epithelial cells. there is also evidence for deregulated hpv-16 e6-e7 mrna stability after integration and specific alterations of host cellular gene expression have been detected upon hpv genome integration. currently, integration of hpv is considered to be an important genetic alteration for the progression of intraepithelial lesions to invasive disease with potential clinical applications like mark tumour progression and diagnostic tool.