PMID- 21371157
OWN - NLM
STAT- MEDLINE
DCOM- 20111223
LR  - 20211020
IS  - 1750-3639 (Electronic)
IS  - 1015-6305 (Print)
IS  - 1015-6305 (Linking)
VI  - 21
IP  - 5
DP  - 2011 Sep
TI  - Chronic progressive deficits in neuron size, density and number in the trigeminal 
      ganglia of mice latently infected with herpes simplex virus.
PG  - 583-93
LID - 10.1111/j.1750-3639.2011.00485.x [doi]
AB  - Numerous epidemiological studies have proposed a link between herpes simplex 
      virus (HSV) infection and several common chronic neuropsychiatric and 
      neurodegenerative diseases. Experimental HSV infection of mice can lead to 
      chronic behavioral and neurological deficits and chronic pain. While neuron 
      injury and loss are well-documented consequences of the acute phase of infection, 
      the pathologic consequences of latent HSV infection are poorly understood. To 
      determine whether latent HSV infection can cause neuronal injury in mice, 
      trigeminal ganglia (TG) derived from adult BALB/c mice 1, 12 and 31 weeks after 
      corneal HSV type 1 (HSV-1) inoculation were analyzed for evidence of productive 
      or latent HSV-1 infection, inflammation and changes in neuron size, density and 
      number. We found that latent HSV-1 infection between 12 and 31 weeks after 
      corneal virus inoculation was associated with inflammation and progressive 
      deficits in mean neuron diameter, neuronal nucleus diameter, neuron density and 
      neuron number in the TG relative to mock-infected controls. The extent of 
      neuronal injury during latent infection correlated with the extent of 
      inflammation. These studies demonstrate that latent HSV infection is associated 
      with progressive neuronal pathology and may lead to a better understanding of the 
      role of HSV infections in chronic neurological diseases.
CI  - (c) 2011 The Authors. Brain Pathology (c) 2011 International Society of 
      Neuropathology.
FAU - Dosa, Sandor
AU  - Dosa S
AD  - Department of Pathology, University of Illinois at Chicago, College of Medicine, 
      Chicago, IL 60612, USA.
FAU - Castellanos, Karla
AU  - Castellanos K
FAU - Bacsa, Sarolta
AU  - Bacsa S
FAU - Gagyi, Eva
AU  - Gagyi E
FAU - Kovacs, S Krisztian
AU  - Kovacs SK
FAU - Valyi-Nagy, Klara
AU  - Valyi-Nagy K
FAU - Shukla, Deepak
AU  - Shukla D
FAU - Dermody, Terence S
AU  - Dermody TS
FAU - Valyi-Nagy, Tibor
AU  - Valyi-Nagy T
LA  - eng
GR  - R37 AI038296/AI/NIAID NIH HHS/United States
GR  - R37 AI038296-13/AI/NIAID NIH HHS/United States
GR  - R37 AI38296/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20110403
PL  - Switzerland
TA  - Brain Pathol
JT  - Brain pathology (Zurich, Switzerland)
JID - 9216781
RN  - 0 (Adaptor Proteins, Signal Transducing)
RN  - 0 (Lat protein, mouse)
RN  - 0 (Membrane Proteins)
RN  - 0 (Phosphoproteins)
RN  - 0 (Viral Proteins)
SB  - IM
MH  - Adaptor Proteins, Signal Transducing/metabolism
MH  - Age Factors
MH  - Analysis of Variance
MH  - Animals
MH  - Cell Count/methods
MH  - Disease Models, Animal
MH  - Disease Progression
MH  - Female
MH  - Gene Expression Regulation, Viral
MH  - HIV Infections/*pathology
MH  - Herpesvirus 1, Human/*pathogenicity
MH  - Inflammation/etiology/virology
MH  - Membrane Proteins/metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Neurons/*pathology/virology
MH  - Phosphoproteins/metabolism
MH  - Time Factors
MH  - Trigeminal Ganglion/*pathology/virology
MH  - Viral Proteins/metabolism
PMC - PMC3125479
MID - NIHMS277771
EDAT- 2011/03/05 06:00
MHDA- 2011/12/24 06:00
PMCR- 2011/04/03
CRDT- 2011/03/05 06:00
PHST- 2011/03/05 06:00 [entrez]
PHST- 2011/03/05 06:00 [pubmed]
PHST- 2011/12/24 06:00 [medline]
PHST- 2011/04/03 00:00 [pmc-release]
AID - BPA485 [pii]
AID - 10.1111/j.1750-3639.2011.00485.x [doi]
PST - ppublish
SO  - Brain Pathol. 2011 Sep;21(5):583-93. doi: 10.1111/j.1750-3639.2011.00485.x. Epub 
      2011 Apr 3.