Cargando…
Transient Reversal of Episome Silencing Precedes VP16-Dependent Transcription during Reactivation of Latent HSV-1 in Neurons
Herpes simplex virus type-1 (HSV-1) establishes latency in peripheral neurons, creating a permanent source of recurrent infections. The latent genome is assembled into chromatin and lytic cycle genes are silenced. Processes that orchestrate reentry into productive replication (reactivation) remain p...
Autores principales: | Kim, Ju Youn, Mandarino, Angelo, Chao, Moses V., Mohr, Ian, Wilson, Angus C. |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2012
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3285597/ https://www.ncbi.nlm.nih.gov/pubmed/22383875 http://dx.doi.org/10.1371/journal.ppat.1002540 |
Ejemplares similares
-
Host factors associated with either VP16 or VP16‐induced complex differentially affect HSV‐1 lytic infection
por: Ding, Xiuyan, et al.
Publicado: (2022) -
De Novo Synthesis of VP16 Coordinates the Exit from HSV Latency In
Vivo
por: Thompson, Richard L., et al.
Publicado: (2009) -
G-quadruplex-interacting compounds alter latent DNA replication and episomal persistence of KSHV
por: Madireddy, Advaitha, et al.
Publicado: (2016) -
Bacterial episomes and plasmids;
Publicado: (1969) -
The SMC5/6 complex: An emerging antiviral restriction factor that can silence episomal DNA
por: Irwan, Ishak D., et al.
Publicado: (2023)