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. 2012:6:249-56.
doi: 10.2174/1874357901206010249. Epub 2012 Dec 28.

The invisible enemy - how human papillomaviruses avoid recognition and clearance by the host immune system

Agnieszka K Grabowska  1 , Angelika B Riemer
Affiliations

The invisible enemy - how human papillomaviruses avoid recognition and clearance by the host immune system

Agnieszka K Grabowska et al. Open Virol J. 2012.

Abstract

Human papillomavirus (HPV) needs to persist in squamous epithelia for a certain amount of time to complete its reproductive cycle. Therefore, the virus has evolved multiple immune evasion strategies. The interplay of these immune evasion mechanisms with the host immune system decides whether a HPV infection is cleared or becomes persistent. Clearance of HPV-induced lesions is mediated by a cellular immune response, consisting of both cytotoxic T lymphocyte and T helper cell responses. Persistent HPV infection, on the other hand, is the single most important risk factor for the development of HPV-associated premalignant lesions and HPV-driven cancers. This article reviews the immune evasion mechanisms employed by high-risk HPVs to escape host immune recognition and attack.

Keywords: Cancer; human papillomavirus (HPV); immune evasion.; immune response.

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Figures

Fig. (1)
Fig. (1)
Intracellular HPV immune evasion mechanisms. (A) HPV dysregulates the interferon response via interaction with the TYK2 kinase (1) and the p48/IRF9 complex (2), thus inhibiting the formation of the ISGF3 transcription complex that binds ISRE in the nucleus (3). (B) HPV promotes apoptosis resistance through down-regulation of the CD95 receptor on the cell surface and modulation of the DISC formation (1), and by degradation of the pro-apoptotic molecules FADD and procaspase-8 (2). (C) HPV causes reduction of antigen presentation by down-regulation of the antigen processing machinery via inhibition of expression of proteasome subunits (1), MHC class I (2), TAP (3), and reduction of MHC-I trafficking by direct interaction with the MHC-I heavy chain (4) and arresting of MHC-I molecules in the Golgi apparatus (5).
Fig. (2)
Fig. (2)
HPV-mediated effects on the host immune response. (A) Immune evasion mechanisms employed by a HPV-infected cell are polarization of T cell subtypes, inhibition of the CTL response and modulation of APC trafficking. (B) Immune evasion mechanisms of HPV-driven malignantly transformed cells include recruitment of immunosuppressive cells, leading to immunosuppressive cytokine production.
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