Journal
VIROLOGY
Volume 522, Issue -, Pages 81-91Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2018.07.011
Keywords
Herpes simplex virus; Reactivation; Epigenetics; NGF-deprivation; Axotomy; DLK
Categories
Funding
- National Institutes of Health [NS105630]
- training grants [T32GM007267, T32AI007046]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [T32AI007046] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [T32GM007267] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS105630] Funding Source: NIH RePORTER
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Herpes simplex virus (HSV) establishes a latent infection in peripheral neurons and can periodically reactivate to cause disease. Reactivation can be triggered by a variety of stimuli that activate different cellular processes to result in increased HSV lytic gene expression and production of infectious virus. The use of model systems has contributed significantly to our understanding of how reactivation of the virus is triggered by different physiological stimuli that are correlated with recrudescence of human disease. Furthermore, these models have led to the identification of both common and distinct mechanisms of different HSV reactivation pathways. Here, we summarize how the use of these diverse model systems has led to a better understanding of the complexities of HSV reactivation, and we present potential models linking cellular signaling pathways to changes in viral gene expression.
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