Abstract
Herpes simplex virus type 1 (HSV-1) infections represent a significant worldwide heath problem. The lack of an effective therapy to curtail reactivation of HSV-1 from a state of neuronal latency has lead to significant morbidity and mortality. Effective therapies to prevent reactivation must likely elicit a protective CD8 T-cell response that could act to prevent reactivation from sensory neurons prior to release of infectious virus at the periphery. This review focuses on the present understanding of how CD8 T cells maintain HSV-1 latency and how this knowledge could facilitate the generation of more effective therapeutic modalities.
Acknowledgement
The authors would like to thank K Lathrop for technical assistance in generating the figure depicting our working model. BS Sheridan and JE Knickelbein both contributed equally to this work.
Disclosure
The authors have no conflicting financial interests.