Immunity to polyoma virus infection and tumorigenesis

Viral Immunol. 2001;14(3):199-216. doi: 10.1089/088282401753266738.

Abstract

Because oncogenic DNA viruses establish persistent infections in humans, continuous immunosurveillance for neoplastic cells is required to prevent virus-induced tumors. Antigen-specific CD8+ T lymphocytes are critical in vivo effectors for eliminating virus-infected and virus-transformed cells. Investigation into the induction, regulation, and maintenance of CD8+ T cells specific for these viruses is hindered by the lack of tractable animal models that mimic natural infection. Resistance to tumors induced by polyoma virus, a persistent natural mouse DNA virus, is mediated by polyoma-specific CD8+ T cells. Mice susceptible to polyoma virus tumorigenesis mount a smaller, albeit still considerable, expansion of anti-polyoma CD8+ T cells; importantly, these antiviral CD8+ T cells lack cytotoxic activity while retaining the phenotype of cytotoxic T lymphocyte (CTL) effectors. In this review, we will discuss potential in vivo mechanisms that regulate the functional competence of anti-polyoma CD8+ T cells, particularly in the context of chronic antigenic stimulation provided by persistent viral infections and tumors.

Publication types

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

MeSH terms

  • Animals
  • CD8-Positive T-Lymphocytes / immunology*
  • Humans
  • Mice
  • Neoplasms, Experimental / immunology*
  • Polyomavirus / immunology*
  • Polyomavirus Infections / immunology*
  • Tumor Virus Infections / immunology*