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...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Ju Youn Kim, Angelo Mandarino, Moses V Chao, Ian Mohr, Angus C Wilson
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/a581ea214a5f49e8888b2120c9947265
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:a581ea214a5f49e8888b2120c9947265
record_format	dspace
spelling	oai:doaj.org-article:a581ea214a5f49e8888b2120c99472652021-11-18T06:04:44ZTransient reversal of episome silencing precedes VP16-dependent transcription during reactivation of latent HSV-1 in neurons.1553-73661553-737410.1371/journal.ppat.1002540https://doaj.org/article/a581ea214a5f49e8888b2120c99472652012-02-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22383875/pdf/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Herpes 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 poorly understood. We have used latently infected cultures of primary superior cervical ganglion (SCG) sympathetic neurons to profile viral gene expression following a defined reactivation stimulus. Lytic genes are transcribed in two distinct phases, differing in their reliance on protein synthesis, viral DNA replication and the essential initiator protein VP16. The first phase does not require viral proteins and has the appearance of a transient, widespread de-repression of the previously silent lytic genes. This allows synthesis of viral regulatory proteins including VP16, which accumulate in the cytoplasm of the host neuron. During the second phase, VP16 and its cellular cofactor HCF-1, which is also predominantly cytoplasmic, concentrate in the nucleus where they assemble an activator complex on viral promoters. The transactivation function supplied by VP16 promotes increased viral lytic gene transcription leading to the onset of genome amplification and the production of infectious viral particles. Thus regulated localization of de novo synthesized VP16 is likely to be a critical determinant of HSV-1 reactivation in sympathetic neurons.Ju Youn KimAngelo MandarinoMoses V ChaoIan MohrAngus C WilsonPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 8, Iss 2, p e1002540 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
spellingShingle	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 Ju Youn Kim Angelo Mandarino Moses V Chao Ian Mohr Angus C Wilson Transient reversal of episome silencing precedes VP16-dependent transcription during reactivation of latent HSV-1 in neurons.
description	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 poorly understood. We have used latently infected cultures of primary superior cervical ganglion (SCG) sympathetic neurons to profile viral gene expression following a defined reactivation stimulus. Lytic genes are transcribed in two distinct phases, differing in their reliance on protein synthesis, viral DNA replication and the essential initiator protein VP16. The first phase does not require viral proteins and has the appearance of a transient, widespread de-repression of the previously silent lytic genes. This allows synthesis of viral regulatory proteins including VP16, which accumulate in the cytoplasm of the host neuron. During the second phase, VP16 and its cellular cofactor HCF-1, which is also predominantly cytoplasmic, concentrate in the nucleus where they assemble an activator complex on viral promoters. The transactivation function supplied by VP16 promotes increased viral lytic gene transcription leading to the onset of genome amplification and the production of infectious viral particles. Thus regulated localization of de novo synthesized VP16 is likely to be a critical determinant of HSV-1 reactivation in sympathetic neurons.
format	article
author	Ju Youn Kim Angelo Mandarino Moses V Chao Ian Mohr Angus C Wilson
author_facet	Ju Youn Kim Angelo Mandarino Moses V Chao Ian Mohr Angus C Wilson
author_sort	Ju Youn Kim
title	Transient reversal of episome silencing precedes VP16-dependent transcription during reactivation of latent HSV-1 in neurons.
title_short	Transient reversal of episome silencing precedes VP16-dependent transcription during reactivation of latent HSV-1 in neurons.
title_full	Transient reversal of episome silencing precedes VP16-dependent transcription during reactivation of latent HSV-1 in neurons.
title_fullStr	Transient reversal of episome silencing precedes VP16-dependent transcription during reactivation of latent HSV-1 in neurons.
title_full_unstemmed	Transient reversal of episome silencing precedes VP16-dependent transcription during reactivation of latent HSV-1 in neurons.
title_sort	transient reversal of episome silencing precedes vp16-dependent transcription during reactivation of latent hsv-1 in neurons.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/a581ea214a5f49e8888b2120c9947265
work_keys_str_mv	AT juyounkim transientreversalofepisomesilencingprecedesvp16dependenttranscriptionduringreactivationoflatenthsv1inneurons AT angelomandarino transientreversalofepisomesilencingprecedesvp16dependenttranscriptionduringreactivationoflatenthsv1inneurons AT mosesvchao transientreversalofepisomesilencingprecedesvp16dependenttranscriptionduringreactivationoflatenthsv1inneurons AT ianmohr transientreversalofepisomesilencingprecedesvp16dependenttranscriptionduringreactivationoflatenthsv1inneurons AT anguscwilson transientreversalofepisomesilencingprecedesvp16dependenttranscriptionduringreactivationoflatenthsv1inneurons
_version_	1718424624034742272

Transient reversal of episome silencing precedes VP16-dependent transcription during reactivation of latent HSV-1 in neurons.

Ejemplares similares