期刊
VIRUS RESEARCH
卷 231, 期 -, 页码 21-33出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.virusres.2016.11.023
关键词
Papillomavirus; HPV; Tumor virus; Oncogene; Immune evasion; Virus evolution; Restriction factor; Innate immunity; Adaptive immunity; DNA methylation; Histone modification; APOBEC3
类别
资金
- National Institutes of Health [R01 AI091968, R01 DE026125]
- Mary Kay Foundation, Dallas, TX [041-15]
- Colorado Clinical and Translational Sciences Institute
- Cancer League of Colorado [163354-DP]
A majority of human papillomavirus (HPV) infections are asymptomatic and self-resolving in the absence of medical interventions. Various innate and adaptive immune responses, as well as physical barriers, have been implicated in controlling early HPV infections. However, if HPV overcomes these host immune defenses and establishes persistence in basal keratinocytes, it becomes very difficult for the host to eliminate the infection. The HPV oncoproteins ES, E6, and E7 are important in regulating host immune responses. These oncoproteins dysregulate gene expression, protein-protein interactions, posttranslational modifications, and cellular trafficking of critical host immune modulators. In addition to the HPV oncoproteins, sequence variation and dinucleotide depletion in papillomavirus genomes has been suggested as an alternative strategy for evasion of host immune defenses. Since anti-HPV host immune responses are also considered to be important for antitumor immunity, immune dysregulation by HPV during virus persistence may contribute to immune suppression essential for HPV-associated cancer progression. Here, we discuss cellular pathways dysregulated by HPV that allow the virus to evade various host immune defenses. (C) 2016 The Authors. Published by Elsevier B.V.
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