Abstract
Herpes simplex virus 1 (HSV-1) is a human pathogen that establishes latency in the nucleus of infected neurons in the PNS and the CNS. At the transcriptional level latency is characterized by a quasi-complete silencing of the extrachromosomal viral genome that otherwise expresses more than 80 genes during the lytic cycle. In neurons, latency is anticipated to be the default transcriptional program; however, limited information exists on the molecular mechanisms that force the virus to enter the latent state. Our recent study demonstrates that the interaction of the viral genomes with the nuclear architecture and specifically the promyelocytic leukemia nuclear bodies (PML-NBs) is a major determinant for the entry of HSV-1 into latency (Maroui MA, Callé A et al. (2016). Latency entry of herpes simplex virus 1 is determined by the interaction of its genome with the nuclear environment. PLoS Pathogens 12(9): e1005834.).
Highlights
Herpes simplex virus 1 (HSV-1) is a human pathogen that establishes latency in the nucleus of infected neurons in the PNS and the CNS
Our recent study demonstrates that the interaction of the viral genomes with the nuclear architecture and the promyelocytic leukemia nuclear bodies (PML-NBs) is a major determinant for the entry of HSV-1 into latency (Maroui MA, Callé A et al (2016)
Latency entry of herpes simplex virus 1 is determined by the interaction of its genome with the nuclear environment
Summary
The interaction between herpes simplex virus 1 genome and promyelocytic leukemia nuclear bodies (PML-NBs) as a hallmark of the entry in latency Herpes simplex virus 1 (HSV-1) is a human pathogen that establishes latency in the nucleus of infected neurons in the PNS and the CNS.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.