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

Springer Science and Business Media LLC - Tập 36 Số 1 - Trang 119-126 - 2006
Divito, Sherrie1,2,3,4,5, Cherpes, Thomas L.1,2,3,4,5, Hendricks, Robert L.1,2,3,4,5
1Graduate Program in Immunology, Magee-Womens Hospital, Pittsburgh
2Department of Obstetrics, Gynecology and Reproductive Sciences, Magee-Womens Hospital, Pittsburgh
3Department of Ophthalmology, University of Pittsburgh, Pittsburgh
4Department of Immunology, University of Pittsburgh, Pittsburgh
5Molecular Genetics and Biochemistry, University of Pittsburgh, Pittsburgh

Tóm tắt

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.

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