INTRODUCTIONHuman papillomaviruses (HPVs) consist of a heterogeneous group of non‐enveloped, capsid‐enclosed dsDNA viruses, 55 nm in diameter that exhibit a different tropism for mucosal or cutaneous epithelia. Today more than 170 HPV genotypes have been completely characterized with each one of them displaying different life cycle features and carcinogenic properties. A phylogenetic tree based on the L1 gene clustered the different HPV genotypes into five genera—alpha, beta, gamma, mu, and nu. The Alphapapillomaviruses can be further sub‐divided into high‐risk (HR) genotypes and low‐risk (LR) genotypes considering their epidemiological association with neoplastic disease. Persistent infection with high‐risk HPV genotypes is regarded as the most crucial risk factor for cervical cancer development. Cancer of the uterine cervix is the third most common malignancy in women in terms of incidence and mortality rates and it is the second leading cause of cancer‐associated deaths, worldwide, with higher frequency in low‐income countries. Global epidemiological investigations have indicated that HPV16 and HPV18 are the most tumorigenic genotypes and they are responsible for approximately 50% and 20% of cervical cancer cases, respectively.The high expression level of high‐risk E6 and E7 oncoproteins is the biological hallmark for initiation of neoplastic disease, since they target and inactivate the cell‐cycle
Journal of Medical Virology – Wiley
Published: Jan 1, 2018
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