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The pathogenesis of pseudorabies in mice: virus replication at the inoculation site and axonal uptake
Abstract:
Three-week-old mice were inoculated in the right ear pinna with pseuforabies virus. Ears were surgically removed at various times after inoculation and changes from the normal pathogenesis were observed. Virus replication in the ear tissue and cervical dorsal root ganglia was also monitored. Followed inoculation with a small dose of virus, local multiplication of the virus was necessary before the infection spread to the nerves. With larger infecting doses there was probably direct uptake of virus from the inoculum into the nerve endings. After these larger doses virus was first detected in the dorsal root ganglia 17 h agter infection, suggesting a retrograde axonal flow rate of at lease 1-7 mm/h.
Insights
Pseudorabies virus infection in mice shows that local virus multiplication is needed for nerve spread with small doses. Larger doses allow direct nerve uptake, with virus reaching ganglia in 17 hours, indicating rapid retrograde axonal flow.
Area of Science:
- Virology
- Neuroscience
- Pathogenesis
Background:
- Pseudorabies virus (PRV) is a significant pathogen affecting swine.
- Understanding PRV neurotropism is crucial for disease control and prevention.
Purpose of the Study:
- To investigate the early pathogenesis of pseudorabies virus infection in the mouse ear pinna.
- To determine the route and rate of viral spread from the inoculation site to the nervous system.
Main Methods:
- Three-week-old mice were inoculated with pseudorabies virus in the ear pinna.
- Ears were surgically removed at various time points post-inoculation.
- Virus replication was monitored in ear tissue and cervical dorsal root ganglia.
Main Results:
- Small PRV doses required local replication before spread to nerves.
- Large PRV doses likely involved direct uptake into nerve endings.
- Virus detected in dorsal root ganglia 17 hours post-infection with large doses.
- Estimated retrograde axonal flow rate of at least 1.7 mm/h.
Conclusions:
- The route of PRV neuroinvasion depends on the inoculum dose.
- Rapid retrograde axonal transport facilitates early spread of PRV to the central nervous system.