“…It is these genotypic differences that permit stratification of the virus oncogenic phenotype into high and low-risk types. High risk includes HPV- 16,18,31,33,35,45,51,52,56,58,59 and low risk are HPV 6,11,42,43,44.The molecular mechanisms by which HPVs disrupt key cellular elements responsible for cell cycle regulation and apoptosis have been identified. [33,34] Degradation of p53 by the E6 protein of HR-HPV is also one of the mechanisms by which the normal function of p53 is altered in HPV-associated oral carcinogenesis.…”