PMID- 32226020
OWN - NLM
STAT- MEDLINE
DCOM- 20200629
LR  - 20240425
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 15
IP  - 3
DP  - 2020
TI  - Herpes simplex virus 1 regulates beta-catenin expression in TG neurons during the 
      latency-reactivation cycle.
PG  - e0230870
LID - 10.1371/journal.pone.0230870 [doi]
LID - e0230870
AB  - 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/beta-catenin signaling pathway is differentially expressed in 
      TG during the bovine herpesvirus 1 latency-reactivation cycle. Hence, we 
      hypothesized HSV-1 regulates the Wnt/beta-catenin pathway and promotes maintenance 
      of latency because this pathway enhances neuronal survival and axonal repair. New 
      studies revealed beta-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 beta-catenin+ TG 
      neurons were detected. Conversely, TG explants from uninfected mice or mice 
      latently infected with a LAT-/- mutant increased the number of beta-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 beta-catenin was 
      differentially expressed during the latency-reactivation cycle, in part due to 
      LAT expression.
FAU - Harrison, Kelly S
AU  - Harrison KS
AUID- ORCID: 0000-0003-0211-8769
AD  - Department of Veterinary Pathobiology, College of Veterinary Medicine, Oklahoma 
      State University, Stillwater, OK, United States of America.
FAU - Zhu, Liqian
AU  - Zhu L
AD  - Department of Veterinary Pathobiology, College of Veterinary Medicine, Oklahoma 
      State University, Stillwater, OK, United States of America.
AD  - College of Veterinary Medicine and Jiangsu Co-innovation Center for Prevention 
      and Control of Important Animal Infectious Diseases and Zoonosis, Yangzhou 
      University, Yangzhou, China.
FAU - Thunuguntla, Prasanth
AU  - Thunuguntla P
AD  - Department of Veterinary Pathobiology, College of Veterinary Medicine, Oklahoma 
      State University, Stillwater, OK, United States of America.
FAU - Jones, Clinton
AU  - Jones C
AUID- ORCID: 0000-0002-6656-4971
AD  - Department of Veterinary Pathobiology, College of Veterinary Medicine, Oklahoma 
      State University, Stillwater, OK, United States of America.
LA  - eng
GR  - P20 GM103648/GM/NIGMS NIH HHS/United States
GR  - R01 NS111167/NS/NINDS NIH HHS/United States
GR  - R21 NS102290/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20200330
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (beta Catenin)
SB  - IM
MH  - Animals
MH  - Female
MH  - *Gene Expression Regulation
MH  - Herpesvirus 1, Human/*physiology
MH  - Mice
MH  - Neurons/*metabolism/*virology
MH  - Trigeminal Ganglion/*cytology
MH  - *Virus Activation
MH  - Wnt Signaling Pathway
MH  - beta Catenin/*metabolism
PMC - PMC7105109
COIS- The authors have declared that no competing interests exist.
EDAT- 2020/04/01 06:00
MHDA- 2020/07/01 06:00
PMCR- 2020/03/30
CRDT- 2020/04/01 06:00
PHST- 2019/12/14 00:00 [received]
PHST- 2020/03/10 00:00 [accepted]
PHST- 2020/04/01 06:00 [entrez]
PHST- 2020/04/01 06:00 [pubmed]
PHST- 2020/07/01 06:00 [medline]
PHST- 2020/03/30 00:00 [pmc-release]
AID - PONE-D-19-33585 [pii]
AID - 10.1371/journal.pone.0230870 [doi]
PST - epublish
SO  - PLoS One. 2020 Mar 30;15(3):e0230870. doi: 10.1371/journal.pone.0230870. 
      eCollection 2020.