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Virus-specific cytotoxic lymphocyte response in a neurotropic murine leukemia virus infection
1Retrovirus Research Center, Department of Veterans Affairs Medical Center, Baltimore, MD 21218.
Abstract:
NFS/N mice infected with neurotropic Cas-Br-M murine leukemia virus (MuLV) at 21 days of age were resistant to neurologic disease and demonstrated MuLV-specific cytotoxic T lymphocyte (CTL) activity in spleen cells after in vitro stimulation. NFS/N mice infected with Cas-Br-M MuLV at 2 days of age failed to generate a significant MuLV-specific CTL response and developed neurologic disease 5-8 weeks later. Protection from neurologic disease transferred with fewer in vitro stimulated immune spleen cells than immune T cells from NFS/N mice infected with Cas-Br-M MuLV at 21 days of age. Cas-Br-M MuLV-specific CTL may play an important role in resistance to the paralytic effects of Cas-Br-M MuLV infection by affecting virus dissemination to the central nervous system.
Insights
Mice infected with Cas-Br-M murine leukemia virus (MuLV) at 21 days old resisted neurologic disease due to a cytotoxic T lymphocyte (CTL) response. Early infection at 2 days old prevented CTL generation, leading to disease.
Area of Science:
- Immunology
- Virology
- Neuroscience
Background:
- Murine leukemia virus (MuLV) can cause neurologic disease in susceptible mouse strains.
- The age of infection influences the host's immune response and disease outcome.
Purpose of the Study:
- To investigate the role of cytotoxic T lymphocyte (CTL) responses in resistance to Cas-Br-M MuLV-induced neurologic disease.
- To determine the impact of infection age on CTL generation and protection.
Main Methods:
- NFS/N mice were infected with Cas-Br-M MuLV at different ages (2 days vs. 21 days).
- MuLV-specific CTL activity was assessed in spleen cells after in vitro stimulation.
- Protection from neurologic disease was evaluated and correlated with CTL activity.
Main Results:
- Mice infected at 21 days of age were resistant to neurologic disease and showed significant MuLV-specific CTL activity.
- Mice infected at 2 days of age failed to generate a robust CTL response and developed neurologic disease.
- Transfer of immune spleen cells conferred protection, with fewer cells needed from older-infected mice.
Conclusions:
- MuLV-specific CTLs play a crucial role in conferring resistance to Cas-Br-M MuLV-induced neurologic disease.
- Age at infection is a critical factor determining the development of protective CTL responses and disease outcome.
- CTLs may protect by limiting virus dissemination to the central nervous system.