Potential strategies utilised by papillomavirus to evade host immunity

The co‐evolution of papillomaviruses (PV) and their mammalian hosts has produced mechanisms by which PV might avoid specific and non‐specific host immune responses. Low level expression of PV proteins in infected basal epithelial cells, together with an absence of inflammation and of virus‐induced c...

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Published in:Immunological reviews 1999-04, Vol.168 (1), p.131-142
Main Authors: Frazer, Ian H., Thomas, Ranjeny, Zhou, Jian, Leggatt, Graham R., Dunn, Linda, McMillan, Nigel, Tindle, Robert W., Filgueira, Luis, Manders, Peter, Barnard, Paula, Sharkey, Michael
Format: Article
Language:English
Subjects:
Animals
Epithelial Cells - immunology
Epithelial Cells - virology
Hematopoietic Stem Cells - immunology
Humans
Interferon-alpha - immunology
Keratinocytes - immunology
Keratinocytes - virology
Oncogene Proteins, Viral - immunology
Papillomaviridae - immunology
papillomavirus
Papillomavirus E7 Proteins
Papillomavirus Infections - immunology
T-Lymphocytes, Cytotoxic - immunology
Tumor Virus Infections - immunology
Viral Proteins - immunology
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Summary:The co‐evolution of papillomaviruses (PV) and their mammalian hosts has produced mechanisms by which PV might avoid specific and non‐specific host immune responses. Low level expression of PV proteins in infected basal epithelial cells, together with an absence of inflammation and of virus‐induced cell lysis, restricts the opportunity for effective PV protein presentation to immunocytes by dendritic cells. Additionally, PV early proteins, by a range of mechanisms, may restrict the efficacy of antigen presentation by these cells. Should an immune response be induced lo PV antigens, resting keratinocytes (KC) appear resistant to interferon‐γ‐enhanced mechanisms of cytotoxic T‐lymphocyte (CTL)‐mediated lysis, and expression of PV antigens by resting KC can tolerise PV‐specific CTL. Thus, KC, in the absence of inflammation, may represent an immunologically privileged site for PV infection. Together, these mechanisms play a part in allowing persistence of PV‐induced proliferative skin lesions for months to years, even in immunocompetent hosts.
ISSN:0105-2896
1600-065X
DOI:10.1111/j.1600-065X.1999.tb01288.x