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High-Risk Human Papillomavirus Targets Crossroads in Immune Signaling

Department of Clinical Oncology, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, The Netherlands
Author to whom correspondence should be addressed.
Academic Editor: Joanna Parish
Viruses 2015, 7(5), 2485-2506;
Received: 19 March 2015 / Accepted: 8 May 2015 / Published: 21 May 2015
(This article belongs to the Special Issue Tumour Viruses)
Persistent infections with a high-risk type human papillomavirus (hrHPV) can progress to cancer. High-risk HPVs infect keratinocytes (KCs) and successfully suppress host immunity for up to two years despite the fact that KCs are well equipped to detect and initiate immune responses to invading pathogens. Viral persistence is achieved by active interference with KCs innate and adaptive immune mechanisms. To this end hrHPV utilizes proteins encoded by its viral genome, as well as exploits cellular proteins to interfere with signaling of innate and adaptive immune pathways. This results in impairment of interferon and pro-inflammatory cytokine production and subsequent immune cell attraction, as well as resistance to incoming signals from the immune system. Furthermore, hrHPV avoids the killing of infected cells by interfering with antigen presentation to antigen-specific cytotoxic T lymphocytes. Thus, hrHPV has evolved multiple mechanisms to avoid detection and clearance by both the innate and adaptive immune system, the molecular mechanisms of which will be dealt with in detail in this review. View Full-Text
Keywords: high-risk human papillomavirus; keratinocyte; immune evasion high-risk human papillomavirus; keratinocyte; immune evasion
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Tummers, B.; Van der Burg, S.H. High-Risk Human Papillomavirus Targets Crossroads in Immune Signaling. Viruses 2015, 7, 2485-2506.

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