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Critical role of microRNA-155 in herpes simplex encephalitis

Siddheshvar Bhela1, Sachin Mulik, Pradeep B J Reddy

  • 1Department of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996-0845.

Journal of Immunology (Baltimore, Md. : 1950)
|February 12, 2014
PubMed

Insights

MicroRNA-155 deficiency in mice increases susceptibility to herpes simplex encephalitis (HSE). Impaired CD8 T cell responses explain this heightened vulnerability and reduced viral latency.

Area of Science:

  • Immunology
  • Virology
  • Neuroscience

Background:

  • Herpes simplex encephalitis (HSE) is a severe complication of HSV infection in humans.
  • The underlying mechanisms contributing to HSE development remain incompletely understood.
  • MicroRNA-155 knockout (miR-155KO) mice offer a potential model for studying HSE.

Purpose of the Study:

  • To investigate the role of microRNA-155 (miR-155) in susceptibility to herpes simplex virus type 1 (HSV-1) infection and HSE.
  • To elucidate the impact of miR-155 deficiency on immune responses, particularly CD8 T cells, during HSV-1 infection.
  • To assess the influence of miR-155 on viral latency and dissemination within the nervous system.

Main Methods:

  • Ocular infection of miR-155KO mice and wild-type controls with HSV-1.
  • Assessment of HSE development, lesion severity, and survival rates.
  • Evaluation of CD8 T cell numbers, functionality, and homing capacity.
  • Adoptive transfer of HSV-immune CD8 T cells into infected miR-155KO mice.
  • Analysis of viral latency and dissemination in the nervous system.

Main Results:

  • miR-155KO mice exhibited significantly higher susceptibility to HSE (75-80% incidence) after ocular HSV-1 infection.
  • Acyclovir treatment protected miR-155KO mice from HSE when administered 4 days post-infection.
  • miR-155 deficiency led to diminished CD8 T cell responses, affecting their numbers, function, and homing.
  • Adoptive transfer of CD8 T cells conferred protection against HSE in infected miR-155KO mice.
  • miR-155KO animals showed impaired ability to maintain HSV latency.

Conclusions:

  • miR-155 plays a critical role in controlling HSV-1 infection and preventing HSE.
  • Impaired CD8 T cell immunity in miR-155 deficient mice underlies their increased susceptibility to HSE and zosteriform lesions.
  • This study establishes a link between miR-155 expression and nervous system susceptibility to viral infections, offering insights into HSE pathogenesis.

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