Potential strategies utilised by papillomavirus to evade host immunity

Immunol Rev. 1999 Apr;168:131-42. doi: 10.1111/j.1600-065x.1999.tb01288.x.

Abstract

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 to PV antigens, resting keratinocytes (KC) appear resistant to interferon-gamma-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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • 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 E7 Proteins
  • Papillomavirus Infections / immunology*
  • T-Lymphocytes, Cytotoxic / immunology
  • Tumor Virus Infections / immunology*
  • Viral Proteins / immunology

Substances

  • Interferon-alpha
  • Oncogene Proteins, Viral
  • Papillomavirus E7 Proteins
  • Viral Proteins
  • oncogene protein E7, Human papillomavirus type 16