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A triple entente: virus, neurons, and CD8+ T cells maintain HSV-1 latency.

TitleA triple entente: virus, neurons, and CD8+ T cells maintain HSV-1 latency.
Publication TypeJournal Article
Year of Publication2006
AuthorsDivito S, Cherpes TL, Hendricks RL
JournalImmunol Res
Volume36
Issue1-3
Pagination119-26
Date Published2006
ISSN0257-277X
KeywordsAnimals, CD8-Positive T-Lymphocytes, Herpes Simplex, Herpesvirus 1, Human, Humans, Interferon-gamma, Models, Immunological, Neurons, Virus Activation, Virus Latency
Abstract

<p>Herpes simplex virus type 1 (HSV-1) travels by retrograde transport to sensory ganglia where latency is established. Recurrent disease results from virus reactivation and anterograde transport to nerve termini. Prevention of reactivation requires a complex interplay among virus, neuron, and immune response. Study of this tripartite relationship suggests possible interaction, and even communication among these components, that direct an immune response that allows for control of virus while preserving the viability of host tissue. Exciting new evidence supports the view that CD8+ effector T cells employ both lytic granule-dependent and interferon gamma-dependent effector mechanisms in maintaining HSV-1 latency.</p>

DOI10.1385/IR:36:1:119
Alternate JournalImmunol. Res.
Citation KeyCK97
PubMed ID17337772