Home News About Us Contact Contributors Disclaimer Privacy Policy Help FAQ

Home
Search
Quick Search
Advanced
Fulltext
Browse
Collections
Persons
My eDoc
Session History
Login
Name:
Password:
Documentation
Help
Support Wiki
Direct access to
document ID:


          Institute: MPI für Neurobiologie     Collection: Neuroimmunology     Display Documents



  history
ID: 127419.0, MPI für Neurobiologie / Neuroimmunology
Latent herpesvirus infection in human trigeminal ganglia causes chronic immune response
Authors:Theil, Diethilde; Derfuss, Tobias; Paripovic, I.; Herberger, Simone; Meinl, Edgar; Schueler, O.; Strupp, M.; Arbusow, V.; Brandt, T.
Language:English
Date of Publication (YYYY-MM-DD):2003-12
Title of Journal:American Journal of Pathology
Journal Abbrev.:Am. J. Pathol.
Volume:163
Issue / Number:6
Start Page:2179
End Page:2184
Review Status:Peer-review
Audience:Not Specified
Abstract / Description:The majority of trigeminal ganglia (TGs) are latently infected with a-herpesviruses [herpes simplex virus type-1 (HSV-1) and varicella-zoster virus (VZV)]. Whereas HSV-1 periodically reactivates in the TGs, VZV reactivates very rarely. The goal of this study was to determine whether herpesvirus latency is linked to a local immune cell infiltration in human TGs. T cells positive for the CD3 and CD8 markers, and CD68-positive macrophages were found in 30 of 42 examined TGs from 21 healthy individuals. The presence of immune cells correlated constantly with the occurrence of the HSV-1 latency-associated transcript (LAT) and only irregularly with the presence of latent VZV protein. In contrast, uninfected TGs showed no immune cell infiltration. Quantitative RT-PCR revealed that CD8, interferon-gamma, tumor necrosis factor-alpha, IP-10, and RANTES transcripts were significantly induced in TGs latently infected with HSV-1 but not in uninfected TGs. The persisting lymphocytic cell infiltration and the elevated CD8 and cytokine/chemokine expression in the TGs demonstrate for the first time that latent herpesviral infection in humans is accompanied by a chronic inflammatory process at an immunoprivileged site but without any neuronal destruction. The chronic immune response seems to maintain viral latency and influence viral reactivation.
Comment of the Author/Creator:Date: 2003, DEC
External Publication Status:published
Document Type:Article
Affiliations:MPI für Neurobiologie/Neuroimmunology (Wekerle)/Clinical Neuroimmunology (Hohlfeld)
External Affiliations:Univ Munich, Klinikum Grosshadern, Dept Neurol, D-81377 Munich, Germany.; Univ Munich, Inst Clin Neuroimmunol, D-81377 Munich, Germany.; Max Planck Inst Neurobiol, Martinsried, Germany.
Identifiers:ISI:000186769800006 [ID No:1]
ISSN:0002-9440 [ID No:2]
The scope and number of records on eDoc is subject to the collection policies defined by each institute - see "info" button in the collection browse view.