Herpes simplex virus 1 regulates β-catenin expression in TG neurons during the latency-reactivation cycle.

When herpes simplex virus 1 (HSV-1) infection is initiated in the ocular, nasal, or oral cavity, sensory neurons within trigeminal ganglia (TG) become infected. Following a burst of viral transcription in TG neurons, lytic cycle viral genes are suppressed and latency is established. The latency-asso...

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Autores principales:	Kelly S Harrison, Liqian Zhu, Prasanth Thunuguntla, Clinton Jones
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2020
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/95f6635f22ee48a89085a09e829cac6c
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spelling	oai:doaj.org-article:95f6635f22ee48a89085a09e829cac6c2021-12-02T20:05:47ZHerpes simplex virus 1 regulates β-catenin expression in TG neurons during the latency-reactivation cycle.1932-620310.1371/journal.pone.0230870https://doaj.org/article/95f6635f22ee48a89085a09e829cac6c2020-01-01T00:00:00Zhttps://doi.org/10.1371/journal.pone.0230870https://doaj.org/toc/1932-6203When herpes simplex virus 1 (HSV-1) infection is initiated in the ocular, nasal, or oral cavity, sensory neurons within trigeminal ganglia (TG) become infected. Following a burst of viral transcription in TG neurons, lytic cycle viral genes are suppressed and latency is established. The latency-associated transcript (LAT) is the only viral gene abundantly expressed during latency, and LAT expression is important for the latency-reactivation cycle. Reactivation from latency is required for virus transmission and recurrent disease, including encephalitis. The Wnt/β-catenin signaling pathway is differentially expressed in TG during the bovine herpesvirus 1 latency-reactivation cycle. Hence, we hypothesized HSV-1 regulates the Wnt/β-catenin pathway and promotes maintenance of latency because this pathway enhances neuronal survival and axonal repair. New studies revealed β-catenin was expressed in significantly more TG neurons during latency compared to TG from uninfected mice or mice latently infected with a LAT-/- mutant virus. When TG explants were incubated with media containing dexamethasone to stimulate reactivation, significantly fewer β-catenin+ TG neurons were detected. Conversely, TG explants from uninfected mice or mice latently infected with a LAT-/- mutant increased the number of β-catenin+ TG neurons in the presence of DEX relative to samples not treated with DEX. Impairing Wnt signaling with small molecule antagonists reduced virus shedding during explant-induced reactivation. These studies suggested β-catenin was differentially expressed during the latency-reactivation cycle, in part due to LAT expression.Kelly S HarrisonLiqian ZhuPrasanth ThunuguntlaClinton JonesPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 15, Iss 3, p e0230870 (2020)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Kelly S Harrison Liqian Zhu Prasanth Thunuguntla Clinton Jones Herpes simplex virus 1 regulates β-catenin expression in TG neurons during the latency-reactivation cycle.
description	When herpes simplex virus 1 (HSV-1) infection is initiated in the ocular, nasal, or oral cavity, sensory neurons within trigeminal ganglia (TG) become infected. Following a burst of viral transcription in TG neurons, lytic cycle viral genes are suppressed and latency is established. The latency-associated transcript (LAT) is the only viral gene abundantly expressed during latency, and LAT expression is important for the latency-reactivation cycle. Reactivation from latency is required for virus transmission and recurrent disease, including encephalitis. The Wnt/β-catenin signaling pathway is differentially expressed in TG during the bovine herpesvirus 1 latency-reactivation cycle. Hence, we hypothesized HSV-1 regulates the Wnt/β-catenin pathway and promotes maintenance of latency because this pathway enhances neuronal survival and axonal repair. New studies revealed β-catenin was expressed in significantly more TG neurons during latency compared to TG from uninfected mice or mice latently infected with a LAT-/- mutant virus. When TG explants were incubated with media containing dexamethasone to stimulate reactivation, significantly fewer β-catenin+ TG neurons were detected. Conversely, TG explants from uninfected mice or mice latently infected with a LAT-/- mutant increased the number of β-catenin+ TG neurons in the presence of DEX relative to samples not treated with DEX. Impairing Wnt signaling with small molecule antagonists reduced virus shedding during explant-induced reactivation. These studies suggested β-catenin was differentially expressed during the latency-reactivation cycle, in part due to LAT expression.
format	article
author	Kelly S Harrison Liqian Zhu Prasanth Thunuguntla Clinton Jones
author_facet	Kelly S Harrison Liqian Zhu Prasanth Thunuguntla Clinton Jones
author_sort	Kelly S Harrison
title	Herpes simplex virus 1 regulates β-catenin expression in TG neurons during the latency-reactivation cycle.
title_short	Herpes simplex virus 1 regulates β-catenin expression in TG neurons during the latency-reactivation cycle.
title_full	Herpes simplex virus 1 regulates β-catenin expression in TG neurons during the latency-reactivation cycle.
title_fullStr	Herpes simplex virus 1 regulates β-catenin expression in TG neurons during the latency-reactivation cycle.
title_full_unstemmed	Herpes simplex virus 1 regulates β-catenin expression in TG neurons during the latency-reactivation cycle.
title_sort	herpes simplex virus 1 regulates β-catenin expression in tg neurons during the latency-reactivation cycle.
publisher	Public Library of Science (PLoS)
publishDate	2020
url	https://doaj.org/article/95f6635f22ee48a89085a09e829cac6c
work_keys_str_mv	AT kellysharrison herpessimplexvirus1regulatesbcateninexpressionintgneuronsduringthelatencyreactivationcycle AT liqianzhu herpessimplexvirus1regulatesbcateninexpressionintgneuronsduringthelatencyreactivationcycle AT prasanththunuguntla herpessimplexvirus1regulatesbcateninexpressionintgneuronsduringthelatencyreactivationcycle AT clintonjones herpessimplexvirus1regulatesbcateninexpressionintgneuronsduringthelatencyreactivationcycle
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Herpes simplex virus 1 regulates β-catenin expression in TG neurons during the latency-reactivation cycle.

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