Journal
REVIEWS IN MEDICAL VIROLOGY
Volume 32, Issue 6, Pages -Publisher
WILEY
DOI: 10.1002/rmv.2394
Keywords
HSV-1; IE; latency; VP16; VP16-induced complex
Categories
Funding
- Chinese National Science Foundation [31972655, 31772743]
- High-level Talents Research Start-up Project of Hebei University [521100221087]
- NIH-NIAID [R01AI134807]
- Research to Prevent Blindness, Inc.
Ask authors/readers for more resources
HSV-1 is a neurotropic human pathogen that can establish lifelong latency in sensory neurons and cause recurrent disease. VP16, a component of HSV-1 virion, interacts with host factors to stimulate gene transcription and affect host immune responses.
Herpes simplex virus type 1 (HSV-1) is an important human pathogen with neurotropism. Following lytic infection in mucosal or skin epithelium, life-long latency is established mainly in sensory neurons, which can periodically reactivate by stress, leading to recurrent disease and virus transmission. During the virus's productive infection, the tegument protein VP16, a component of HSV-1 virion, is physically associated with two cellular factors, host cell factor-1 (HCF-1), and POU domain protein Oct-1, to construct the VP16-induced complex, which is essential to stimulate immediate early (IE)-gene transcription as well as initiate the lytic programme. Apart from HCF-1 and Oct-1, VP16 also associates with a series of other host factors, making a VP16-induced regulatory switch to either activate or inactivate virus gene transcription. In addition, VP16 has effects on distinct signalling pathways via binding to various host molecules that are essentially related to innate immune responses, RNA polymerases, molecular chaperones, and virus infection-induced host shutoff. VP16 also functionally compensates for given host factors, such as PPAR-gamma and ss-catenin. In this review, we provide an overview of the updated insights on the interplay between VP16 and the host factors that coordinate virus infection.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available