CD8+ T cells patrol HSV-1-infected trigeminal ganglia and prevent viral reactivation

J Neurovirol. 2011 Dec;17(6):528-34. doi: 10.1007/s13365-011-0062-1. Epub 2011 Dec 8.

Abstract

A hallmark of herpes viruses is their capacity to cause recurrent disease. Recurrences of herpes simplex virus (HSV)-1 disease do not result from reinfection from external sources, but rather from reactivation of virus that is maintained in a latent state in sensory neurons and periodically reactivates from latency to cause recurrent disease. Recent findings implicate HSV-specific CD8(+) T cells in immune surveillance of HSV-1 latently infected sensory neurons in trigeminal ganglia (TG) and inhibition of HSV-1 reactivation from latency. This review summarizes recent findings regarding the characteristics of the TG-resident CD8(+) T cell population and certain unique obstacles that might complicate the development of therapeutic vaccines.

Publication types

  • Review

MeSH terms

  • Animals
  • Antigens, Viral / immunology
  • CD8-Positive T-Lymphocytes / immunology*
  • CD8-Positive T-Lymphocytes / virology
  • Cytokines / immunology
  • Gene Expression Regulation, Viral / immunology*
  • Granzymes / immunology
  • Herpes Simplex / immunology*
  • Herpes Simplex / virology
  • Herpesvirus 1, Human / genetics*
  • Herpesvirus 1, Human / immunology
  • Host-Pathogen Interactions
  • Humans
  • Immunity, Innate
  • Mice
  • Mice, Knockout
  • Transcription, Genetic
  • Trigeminal Ganglion / virology*
  • Viral Proteins / genetics
  • Viral Proteins / metabolism*
  • Virus Latency / physiology*

Substances

  • Antigens, Viral
  • Cytokines
  • Viral Proteins
  • Granzymes