A Triple Entente: Virus, Neurons, and CD8+ T Cells Maintain HSV-1 Latency
- 1 January 2006
- journal article
- review article
- Published by Springer Science and Business Media LLC in Immunologic Research
- Vol. 36 (1-3), 119-126
- https://doi.org/10.1385/ir:36:1:119
Abstract
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.Keywords
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