期刊
VIRUS RESEARCH
卷 231, 期 -, 页码 139-147出版社
ELSEVIER
DOI: 10.1016/j.virusres.2016.11.002
关键词
Papillomavirus; HIV; Herpesvirus; Polyomavirus; Parvovirus
类别
资金
- National Institute of General Medical Sciences of the National Institutes of Health [5P30GM11070]
- National Institute for Dental and Craniofacial Research of the National Institutes of Health [R01DE025565]
- LSUHSC-S Feist-Weiller Cancer Center
The etiological role of human papillomavirus (HPV) in anogenital tract and head and neck cancers is well established. However, only a low percentage of HPV-positive women develop cancer, indicating that HPV is necessary but not sufficient in carcinogenesis. Several biological and environmental cofactors have been implicated in the development of HPV-associated carcinoma that include immune status, hormonal changes, parity, dietary habits, tobacco usage, and co-infection with other sexually transmissible agents. Such cofactors likely contribute to HPV persistent infection through diverse mechanisms related to immune control, efficiency of HPV infection, and influences on tumor initiation and progression. Conversely, HPV co-infection with other factors may also harbor anti-tumor effects. Here, we review epidemiological and experimental studies investigating human immunodeficiency virus (HIV), herpes simplex virus (HSV) 1 and 2, human cytomegalovirus (HCMV), Epstein-Barr virus (EBV), BK virus (BIN), JC virus (JCV), and adeno-associated virus (AAV) as viral cofactors in or therapeutic factors against the development of genital and oral HPV-associated carcinomas. (C) 2016 Elsevier B.V. All rights reserved.
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