Herpes Simplex Virus Latency after Direct Ganglion Virus Inoculation
Autor: | Andrew Gaydos, Kathleen A. Hay, Richard B. Tenser, Wade Edris |
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Rok vydání: | 1998 |
Předmět: |
Cell Survival
viruses Acyclovir Gene Expression HSL and HSV Biology Virus Replication medicine.disease_cause Antiviral Agents Immediate-Early Proteins Mice Cellular and Molecular Neuroscience Virus inoculation Ganglia Spinal Virology Chlorocebus aethiops medicine Animals Simplexvirus Latency (engineering) 2-Aminopurine Vero Cells In Situ Hybridization Neurons Mice Inbred BALB C Inoculation Famciclovir RNA Herpes Simplex Viral Load Virus Latency Ganglion medicine.anatomical_structure Herpes simplex virus nervous system Neurology Immunology Axoplasmic transport RNA Viral Neurology (clinical) |
Zdroj: | Journal of Neurovirology. 4:531-538 |
ISSN: | 1538-2443 1355-0284 |
DOI: | 10.3109/13550289809113497 |
Popis: | Herpes simplex virus (HSV) latent infection of ganglion neurons follows axoplasmic transport of HSV, probably in the form of nucleocapsid from peripheral sites of infection (e.g. footpad). This raises the possibility that latency is dependent on this particular means of presenting HSV to ganglion neurons. To investigate this, we directly infected ganglia of mice with HSV and evaluated latency. Initially, ganglia were surgically exposed in intact mice, infected with HSV and after 4 weeks evaluated for HSV latency-associated transcript (LAT) expression. LAT expression suggested latency. To more fully evaluate latency after direct ganglion inoculation, a transplant model was developed. In this model, ganglia were removed from mice, inoculated with HSV, transplanted into syngeneic recipients and evaluated for latency after several weeks. Latency was evident in transplanted ganglia by (1) the presence of LAT in neurons; (2) the lack of HSV ICP4 RNA or viral antigen, and (3) the isolation of HSV from explants of transplants but not from direct homogenates. The transplant model was then used to evaluate the effect of inhibition of HSV replication on latency. Antivirals which inhibited HSV replication markedly decreased the number of LAT-positive neurons in transplants, suggesting a role for HSV replication mechanisms and latency. It is thought that direct ganglion inoculation and ganglion transplant methods will permit unique investigations of mechanisms of latency. |
Databáze: | OpenAIRE |
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