Related Experiment Videos
Neurological involvement in mice after infection with a cold-adapted herpes simplex type 2 virus
Abstract:
Experimental intracerebral infection of 4-week-old mice with the MS strain of herpes simplex virus type 2 or its derivative cold variant was compared. The infectious process was followed in both the brain tissue and the trigeminal ganglia, using hematoxylin and eosin and antigenic tracing with indirect peroxidase-antiperoxidase staining. The wild-type virus elicited a severe meningitis and necrotic lesions by 7 days post-inoculation in the brain. The cold variant produced a mild meningitis and no necrotic lesions. In both viral infections, the neuron seemed to be the target cell at the early stages. Infection with the wild-type strain was able to spread through host tissues and produce confluent lesions, whereas infection with the cold mutant seemed to be confined to individual neurons. Data suggest that the cold variant is restricted in its ability to lyse the cells and spread in the host nervous tissue.
Insights
A cold-variant herpes simplex virus type 2 (HSV-2) caused milder meningitis and restricted spread in mouse nervous tissue compared to wild-type HSV-2. This suggests the cold variant has limited cell lysis and dissemination capabilities.
Area of Science:
- Neurovirology
- Infectious Diseases
- Molecular Virology
Background:
- Herpes simplex virus type 2 (HSV-2) is a neurotropic virus that can cause meningitis and encephalitis.
- Understanding the mechanisms of viral spread and pathogenesis is crucial for developing effective treatments.
Purpose of the Study:
- To compare the neuropathogenesis of wild-type HSV-2 and a cold-variant HSV-2 in a mouse model.
- To investigate the cellular targets and spread patterns of HSV-2 infection in the central nervous system.
Main Methods:
- Intracerebral inoculation of 4-week-old mice with wild-type HSV-2 (MS strain) or its cold variant.
- Histopathological analysis using hematoxylin and eosin staining.
- Antigenic tracing with indirect peroxidase-antiperoxidase staining to track viral spread.
Main Results:
- Wild-type HSV-2 induced severe meningitis and necrotic brain lesions by 7 days post-inoculation.
- The cold variant caused only mild meningitis and no necrotic lesions.
- Neurons were identified as the primary target cells in early stages for both viral strains.
- Wild-type HSV-2 exhibited extensive tissue spread and confluent lesions, while the cold variant's spread was confined to individual neurons.
Conclusions:
- The cold variant of HSV-2 demonstrates significantly reduced virulence and spread within the host nervous system compared to the wild-type strain.
- Data suggest that the cold variant's ability to lyse cells and disseminate is restricted, offering insights into HSV-2 pathogenesis.