Related Experiment Videos
Spread of HSV and establishment of latency after corneal infection in inbred mice
Abstract:
The spread of herpes simplex virus (HSV) through neural tissues was studied in three inbred mouse strains that differ in susceptibility to HSV stromal keratitis. The left eyes of BALB/c, C57BL/6, and DBA/2 mice were inoculated topically with HSV type 1. The optic and trigeminal nerves, trigeminal ganglia, and eyes were assayed for infectious virus on days 1, 2, 3, 4, 7, 9, 11 and 14 after inoculation. At 2-4 months post-inoculation, eyes and trigeminal ganglia were assayed for latent virus. Up to 7 days post-inoculation, infectious virus was present at a similar frequency in the inoculated eyes of mice from all three strains. The quantity of virus recovered, however, was mouse strain-dependent: DBA mice yielded the most virus; C57BL/6, the least. The frequency of virus recovery and the quantity of virus recovered from trigeminal nerves and ganglia also varied according to mouse strain. Infectious virus was recovered from the uninoculated right eye of some DBA and C57BL/6 mice 1 wk after inoculation. The overall incidence of latency differed among inbred mouse strains. However, in mice that developed ocular disease (blepharitis, dendritic keratitis, or stromal keratitis), there was no host strain-related difference in the incidence of latency. These results support the hypothesis that host genetic factors play a role in controlling HSV replication and the spread of virus to neural tissues after ocular HSV inoculation. This control may influence the development and severity of disease. However, once infection occurs, latency is established in both susceptible and resistant mouse strains.
Insights
Host genetic factors influence herpes simplex virus (HSV) spread in neural tissues. While initial infection is similar, mouse strain impacts viral load and latency, affecting disease severity.
Area of Science:
- Virology
- Immunology
- Genetics
Background:
- Herpes simplex virus (HSV) causes ocular infections, including stromal keratitis.
- Susceptibility to HSV stromal keratitis varies among inbred mouse strains.
- Understanding HSV neural spread is crucial for managing ocular disease.
Purpose of the Study:
- To investigate the role of host genetic factors in controlling HSV replication and neural spread.
- To compare HSV-1 dissemination and latency establishment in different mouse strains.
Main Methods:
- Topical ocular inoculation of HSV-1 in BALB/c, C57BL/6, and DBA/2 mice.
- Assay for infectious virus in eyes, optic nerves, trigeminal nerves, and ganglia at multiple time points.
- Assay for latent virus in eyes and trigeminal ganglia 2-4 months post-inoculation.
Main Results:
- Infectious HSV-1 was present in inoculated eyes of all strains up to 7 days.
- Viral quantity recovered varied by strain (DBA > C57BL/6).
- HSV-1 spread to trigeminal nerves/ganglia and contralateral eyes differed among strains.
- Latency incidence varied by strain, but was similar in diseased mice regardless of strain.
Conclusions:
- Host genetic factors significantly control HSV replication and neural tissue spread after ocular inoculation.
- Genetic control influences disease development and severity.
- Latency establishment occurs in both susceptible and resistant mouse strains once infection is established.