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Early replication of Friend leukaemia viruses in spleen macrophages
Abstract:
The ability of spleen macrophages to support Friend leukaemia virus replication was studied by testing for infectivity in adherent cells obtained from mice at various times after infection. Virus-releasing macrophages appeared early after infection and reached a high proportion. The released virus was probably synthesized de novo since macrophage infectivity was strongly reduced by treatments which affected cellular viability or synthetic activities and electron microscopy showed C-type particles budding from macrophages.
Insights
Spleen macrophages rapidly support Friend leukaemia virus replication early after infection. This virus release is likely de novo synthesis, as cellular viability treatments reduce macrophage infectivity.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Friend leukaemia virus (FLV) is an oncogenic retrovirus.
- Macrophages play a critical role in the immune response to viral infections.
Purpose of the Study:
- To investigate the role of spleen macrophages in Friend leukaemia virus replication.
- To determine the kinetics and mechanism of virus release from macrophages.
Main Methods:
- Assessing infectivity of adherent spleen cells from infected mice.
- Treating macrophages to assess effects on viral replication.
- Electron microscopy to visualize viral particles.
Main Results:
- Virus-releasing macrophages were detected early after infection and became abundant.
- Macrophage infectivity was significantly reduced by treatments affecting cellular viability or synthesis.
- Electron microscopy confirmed C-type retroviral particles budding from macrophages.
Conclusions:
- Spleen macrophages are capable of supporting Friend leukaemia virus replication.
- Virus release from macrophages is likely due to de novo synthesis.
- Macrophages are an important cellular component in Friend leukaemia virus infection dynamics.