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HPV16 E7 Genetic Conservation Is Critical to Carcinogenesis.

Mirabello, Lisa; Yeager, Meredith; Yu, Kai; Clifford, Gary M; Xiao, Yanzi; Zhu, Bin; Cullen, Michael; Boland, Joseph F; Wentzensen, Nicolas; Nelson, Chase W; Raine-Bennett, Tina; Chen, Zigui; Bass, Sara; Song, Lei; Yang, Qi; Steinberg, Mia; Burdett, Laurie; Dean, Michael; Roberson, David; Mitchell, Jason; Lorey, Thomas; Franceschi, Silvia; Castle, Philip E; Walker, Joan; Zuna, Rosemary; Kreimer, Aimée R; Beachler, Daniel C; Hildesheim, Allan; Gonzalez, Paula; Porras, Carolina; Burk, Robert D; Schiffman, Mark.
Cell; 170(6): 1164-1174.e6, 2017 Sep 07.
Artigo em Inglês | MEDLINE | ID: mdl-28886384
Although most cervical human papillomavirus type 16 (HPV16) infections become undetectable within 1-2 years, persistent HPV16 causes half of all cervical cancers. We used a novel HPV whole-genome sequencing technique to evaluate an exceptionally large collection of 5,570 HPV16-infected case-control samples to determine whether viral genetic variation influences risk of cervical precancer and cancer. We observed thousands of unique HPV16 genomes; very few women shared the identical HPV16 sequence, which should stimulate a careful re-evaluation of the clinical implications of HPV mutation rates, transmission, clearance, and persistence. In case-control analyses, HPV16 in the controls had significantly more amino acid changing variants throughout the genome. Strikingly, E7 was devoid of variants in precancers/cancers compared to higher levels in the controls; we confirmed this in cancers from around the world. Strict conservation of the 98 amino acids of E7, which disrupts Rb function, is critical for HPV16 carcinogenesis, presenting a highly specific target for etiologic and therapeutic research.
Selo DaSilva