Strategies for immune evasion by human tumor viruses

Curr Opin Virol. 2018 Oct:32:30-39. doi: 10.1016/j.coviro.2018.08.015. Epub 2018 Sep 18.

Abstract

Immune evasion is a hallmark of viral persistence. For the seven human tumor viruses to establish lifelong infection in their hosts, they must successfully control the host response to them. Viral inhibition of immune responses occurs at many levels. While some viruses directly target the pattern recognition receptors (PRR) of the innate immune system, they may also antagonize downstream effectors of PRR signaling cascades or activation of transcription, which would otherwise induce a type I interferon (IFN) and/or pro-inflammatory cytokine response. Secretion of IFN activates the type I interferon receptor (IFNAR) signaling pathway, which is also prone to viral inhibition. To evade the adaptive host response, viruses also target various mechanisms including antigen processing and presentation.

Publication types

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

MeSH terms

  • Adaptive Immunity
  • Antigen Presentation
  • Cytokines / immunology
  • Host-Pathogen Interactions / immunology*
  • Humans
  • Immune Evasion*
  • Immunity, Innate
  • Interferon Type I / immunology
  • Oncogenic Viruses / immunology*
  • Receptor, Interferon alpha-beta / immunology
  • Sarcoma, Kaposi / immunology
  • Sarcoma, Kaposi / virology
  • Signal Transduction
  • Toll-Like Receptors / immunology
  • Tumor Virus Infections / immunology*

Substances

  • Cytokines
  • IFNAR2 protein, human
  • Interferon Type I
  • Toll-Like Receptors
  • Receptor, Interferon alpha-beta