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Updated: Jul 16, 2026

A Primary Neuron Culture System for the Study of Herpes Simplex Virus Latency and Reactivation
Published on: April 2, 2012
A triple entente: virus, neurons, and CD8+ T cells maintain HSV-1 latency
Sherrie Divito1, Thomas L Cherpes, Robert L Hendricks
1Graduate Program in Immunology, University of Pittsburgh, Pittsburgh, PA 15123, USA.
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.
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