Article

Herpes simplex type I (HSV-1) infection of the nervous system: is an immune response a good thing?

Department of Microbiology, Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104, United States.
Journal of neuroimmunology (impact factor: 2.84). 10/2009; 220(1-2):1-9. DOI:10.1016/j.jneuroim.2009.09.013 pp.1-9
Source: PubMed

ABSTRACT Herpes simplex virus type 1 (HSV-1) can induce a robust immune response initially thru the activation of pattern recognition receptors and subsequent type I interferon production that then shapes, along with other innate immune components, the adaptive immune response to the insult. While this response is necessary to quell virus replication, drive the pathogen into a "latent" state, and likely hinder viral reactivation, collateral damage can ensue with demonstrable cell death and foci of tissue pathology in the central nervous system (CNS) as a result of the release of inflammatory mediators including reactive oxygen species. Although rare, HSV-1 is the leading cause of frank sporadic encephalitis that, if left untreated, can result in death. A greater understanding of the contribution of resident glial cells and infiltrating leukocytes within the CNS in response to HSV-1 invasion is necessary to identify candidate molecules as targets for therapeutic intervention to reduce unwarranted inflammation coinciding with the maintenance of the anti-viral state.

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Keywords

adaptive immune response
 
candidate molecules
 
central nervous system
 
CNS
 
foci
 
Herpes simplex virus type 1
 
HSV-1
 
HSV-1 invasion
 
inflammatory mediators
 
latent
 
pattern recognition receptors
 
reactive oxygen species
 
resident glial cells
 
robust immune response
 
subsequent type
 
therapeutic intervention
 
unwarranted inflammation coinciding
 
viral reactivation
 
virus replication