Potential strategies utilised by papillomavirus to evade host immunity

• Published in: Immunological reviews Vol. 168; no. 1; pp. 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: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01-04-1999
• 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
• ISSN: 0105-2896; 1600-065X
• DOI: 10.1111/j.1600-065X.1999.tb01288.x

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.