Innate immune response and viral interference strategies developed by human herpesviruses

Biochem Pharmacol. 2010 Dec 15;80(12):1955-72. doi: 10.1016/j.bcp.2010.07.001. Epub 2010 Jul 8.

Abstract

Viruses are by far the most abundant parasites on earth and they have been found to infect animals, plants and bacteria. However, different types of viruses can only infect a limited range of hosts and many are species-specific. Herpesviruses constitute a large family of DNA viruses that cause diseases in animals, including humans and that are known to undergo lytic or latent infections. Consequently, they developed numerous strategies to counteract host antiviral responses to escape immune surveillance. Innate immune response constitutes the first line of host defence that limits the viral spread and also plays an important role in the activation of adaptive immune response. Viral components are recognized by specific host Pathogen Recognition Receptors (PRRs) which trigger the activation of IRF3, NF-κB and AP-1, three regulators of IFN-β expression. IFN-β is responsible for the induction of Interferon-Stimulated Genes (ISGs) that encode antiviral effectors important to limit the viral spread and to establish an antiviral state as well in the infected cells as in the neighbouring non-infected cells. In this review, we will summarize how host cells recognize viral components and activate downstream signalling pathways leading to the production of IFN-β and ISGs. We will also review the most recent findings in Herpesviruses-encoded proteins involved in host immune evasion.

Publication types

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

MeSH terms

  • Animals
  • Cytomegalovirus / physiology
  • Herpesviridae / physiology*
  • Herpesvirus 1, Human / physiology
  • Herpesvirus 3, Human / physiology
  • Herpesvirus 4, Human / physiology
  • Host-Pathogen Interactions / immunology*
  • Humans
  • Immune Evasion
  • Immunity, Innate*
  • Interferon-beta / biosynthesis
  • Receptors, Virus / physiology
  • Signal Transduction
  • Toll-Like Receptors / physiology

Substances

  • Receptors, Virus
  • Toll-Like Receptors
  • Interferon-beta