Journal
VIRUSES-BASEL
Volume 10, Issue 2, Pages -Publisher
MDPI
DOI: 10.3390/v10020080
Keywords
HPV carcinogenesis; HPV epidemiology; HPV genomics; viral-host interactions; HPV16
Categories
Funding
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health
- National Cancer Institute [CA78527]
- Einstein Cancer Research Center from the National Cancer Institute [P30CA013330]
- Gerstner Family Foundation at the American Museum of Natural History
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Of the similar to 60 human papillomavirus (HPV) genotypes that infect the cervicovaginal epithelium, only 12-13 high-risk types are well-established as causing cervical cancer, with HPV16 accounting for over half of all cases worldwide. While HPV16 is the most important carcinogenic type, variants of HPV16 can differ in their carcinogenicity by 10-fold or more in epidemiologic studies. Strong genotype-phenotype associations embedded in the small 8-kb HPV16 genome motivate molecular studies to understand the underlying molecular mechanisms. Understanding the mechanisms of HPV genomic findings is complicated by the linkage of HPV genome variants. A panel of experts in various disciplines gathered on 21 November 2016 to discuss the interdisciplinary science of HPV oncogenesis. Here, we summarize the discussion of the complexity of the viral-host interaction and highlight important next steps for selected applied basic laboratory studies guided by epidemiological genomic findings.
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