Faculty Collaboration Database

Chronic progressive deficits in neuron size, density and number in the trigeminal ganglia of mice latently infected with herpes simplex virus. Brain Pathol 2011 Sep;21(5):583-93

Date

03/05/2011

Pubmed ID

21371157

Pubmed Central ID

PMC3125479

DOI

10.1111/j.1750-3639.2011.00485.x

Scopus ID

2-s2.0-80052036210 (requires institutional sign-in at Scopus site)   14 Citations

Abstract

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.

Author List

Dosa S, Castellanos K, Bacsa S, Gagyi E, Kovacs SK, Valyi-Nagy K, Shukla D, Dermody TS, Valyi-Nagy T

Author

Sandor K. Kovacs MD Assistant Professor in the Pathology department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Adaptor Proteins, Signal Transducing
Age Factors
Analysis of Variance
Animals
Cell Count
Disease Models, Animal
Disease Progression
Female
Gene Expression Regulation, Viral
HIV Infections
Herpesvirus 1, Human
Inflammation
Membrane Proteins
Mice
Mice, Inbred BALB C
Neurons
Phosphoproteins
Time Factors
Trigeminal Ganglion
Viral Proteins