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

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 t...

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Bibliographic Details
Published in:Journal of neuroimmunology 2010-03, Vol.220 (1), p.1-9
Main Authors: Conrady, Christopher D, Drevets, Douglas A, Carr, Daniel J.J
Format: Article
Language:English
Subjects:
Adaptive Immunity - immunology
Allergy and Immunology
Animals
Antiviral agents
Autoimmune Diseases of the Nervous System - immunology
Autoimmune Diseases of the Nervous System - physiopathology
Autoimmune Diseases of the Nervous System - virology
Brain - immunology
Brain - physiopathology
Brain - virology
Chemotaxis, Leukocyte - immunology
CNS
Encephalitis
Encephalitis - immunology
Encephalitis - physiopathology
Encephalitis - virology
Encephalitis, Herpes Simplex - immunology
Encephalitis, Herpes Simplex - physiopathology
Herpes simplex virus 1
Herpesvirus 1, Human - immunology
HSV-1
Humans
Immune System - physiopathology
Interferons
Neuroglia - immunology
Neurology
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Summary: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.
ISSN:0165-5728
1872-8421
DOI:10.1016/j.jneuroim.2009.09.013