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Laten herpes virus infection in human trigeminal ganglia causes chronic immune response

Posted Jun 10 2009 4:55pm
Am J Pathol. 2003 Dec;163(6):2179-84.

Latent herpesvirus infection in human trigeminal ganglia causes chronic
immune response.

Theil D, Derfuss T, Paripovic I, Herberger S, Meinl E, Schueler O,
Strupp M, Arbusow V, Brandt T. Department of Neurology, Klinikum
Grosshadern, Ludwig-Maximilians University, Munich, Germany.
dtheil@brain.nefo.med.uni-muenchen.de

The majority of trigeminal ganglia (TGs) are latently infected with
alpha-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.

Publication Types:
* Research Support, Non-U.S. Gov't
PMID: 14633592 [PubMed - indexed for MEDLINE]


12: J Immunol. 1996 Oct 15;157(8):3542-9.

Persistent cytokine expression in trigeminal ganglion latently infected
with herpes simplex virus type 1.

Halford WP, Gebhardt BM, Carr DJ. Department of Microbiology,
Louisiana State University Medical Center, New Orleans 70112, USA.

Following ocular infection, herpes simplex virus type 1 (HSV-1)
establishes latency in trigeminal ganglion (TG) neurons. Using reverse
transcription-PCR, cytokine gene expression was analyzed in the TGs of mice
infected with HSV-1. IL-2, TNF-alpha, IFN-gamma, IL-10, and RANTES mRNAs
were readily detected in TGs taken from mice 7 days postinoculation (PI).
Likewise, IL-2, IL-6, IL-10, and IFN-gamma protein were detected by ELISA of
TG homogenates. Between 5 and 45 days PI, IL-10, IFN-gamma, TNF-alpha, and
RANTES mRNAs were detected in nearly 100% of latently infected TGs (latent
infection was confirmed by reverse transcription-PCR detection of HSV-1
latency-associated transcripts). T cell-associated cytokine and chemokine
mRNAs (IL-2, IL-10, IFN-gamma, and RANTES) were still detected in the
majority of latently infected TG samples taken between 60 and 135 days PI.
In contrast, these cytokine mRNA species were rarely detected in uninfected
TGs. Measurement of serum Abs to HSV-1 at different times revealed that
anti-HSV-1 Ab concentrations approached a plateau in mice by 30 days PI but
remained at high levels 67 and 125 days PI. Although there was molecular
evidence of an ongoing immune response to HSV-1 in latently infected TG,
histologic analysis indicated that very few mononuclear cells remained in
the ganglion 60 days PI. Collectively, the results suggest that residual
lymphocytes encounter viral Ag during HSV-1 latency with sufficient
frequency to remain activated. The paradox of a persistent immune response
against a latent infection is discussed.
Publication Types: PMID: 8871654
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