Increased Cell-Mediated Immune Responses in Patients with Recurrent Herpes Simplex Virus Type 2 Meningitis release_e424cc5mu5d6nifl7igskfebna

by Elisabeth Franzen-Röhl, Danika Schepis, Maria Lagrelius, Kristina Franck, Petra Jones, Jan-Åke Liljeqvist, Tomas Bergström, Elisabeth Aurelius, Klas Kärre, Louise Berg, Hans Gaines

Published in Clinical and Vaccine Immunology by American Society for Microbiology.

2011   Volume 18, p655-660

Abstract

<jats:title>ABSTRACT</jats:title>The clinical picture of herpes simplex virus type 2 (HSV-2) infection includes genital blisters and less frequently meningitis, and some individuals suffer from recurrent episodes of these manifestations. We hypothesized that adaptive and/or innate immune functional deficiencies may be a major contributing factor in susceptibility to recurrent HSV-2 meningitis. Ten patients with recurrent HSV-2 meningitis were studied during clinical remission. For comparison, 10 patients with recurrent genital HSV infections as well as 21 HSV-seropositive and 19 HSV-seronegative healthy blood donors were included. HSV-specific T cell blasting and cytokine secretion were evaluated in whole blood cultures. HSV-2-induced NK cell gamma interferon production, dendritic cell Toll-like receptor (TLR) expression, and TLR agonist-induced alpha interferon secretion were analyzed. Patients with recurrent HSV-2 meningitis had elevated T cell blasting and Th1 and Th2 cytokine production in response to HSV antigens compared to those of patients with recurrent genital infections. A somewhat increased NK cell response, increased dendritic cell expression of TLR3 and -9, and increased TLR-induced alpha interferon responses were also noted. Contrary to our expectation, recurrent HSV-2 meningitis patients have increased HSV-specific adaptive and innate immune responses, raising the possibility of immune-mediated pathology in the development of recurrent HSV2 meningitis.
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Type  article-journal
Stage   published
Date   2011-02-16
Language   en ?
DOI  10.1128/cvi.00333-10
PubMed  21325490
PMC  PMC3122567
Wikidata  Q35066312
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