Abstract |
Mortality and morbidity rates remain high among patients with herpes simplex virus encephalitis (HSVE). Chemokine-mediated recruitment and activation of leukocytes to focal areas of viral CNS infection are crucial steps in antiviral response and clearance. However, the inflammatory reaction and cellular antiviral response may enhance collateral damage to neurons and account for chronic progressive brain damage. We identified a specific mRNA expression of the interferon-gamma-inducible chemokines (CXCL9, CXCL10 and CXCL11), and RANTES (CCL5) in the acute course and long-term of experimental HSVE. This pattern was substantially altered by anti-viral and anti-inflammatory treatment. Our findings indicate a pivotal role of these chemokines in the immunopathogenesis of HSVE.
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Authors | Johann Sellner, Florian Dvorak, Yilin Zhou, Jürgen Haas, Roland Kehm, Brigitte Wildemann, Uta Meyding-Lamadè |
Journal | Neuroscience letters
(Neurosci Lett)
Vol. 374
Issue 3
Pg. 197-202
(Feb 21 2005)
ISSN: 0304-3940 [Print] Ireland |
PMID | 15663962
(Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Anti-Inflammatory Agents
- Antiviral Agents
- Chemokines
- RNA, Messenger
- Acyclovir
- Methylprednisolone
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Topics |
- Acyclovir
(therapeutic use)
- Animals
- Anti-Inflammatory Agents
(therapeutic use)
- Antiviral Agents
(therapeutic use)
- Chemokines
(genetics, metabolism)
- Disease Models, Animal
- Drug Interactions
- Drug Therapy, Combination
- Encephalitis, Herpes Simplex
(drug therapy, metabolism)
- Female
- Gene Expression Regulation
(drug effects)
- Methylprednisolone
(therapeutic use)
- Mice
- RNA, Messenger
(metabolism)
- Reverse Transcriptase Polymerase Chain Reaction
(methods)
- Time Factors
- Viral Load
(methods)
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