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Ultrastructural observations of polyoma infected Friend erythroleukemic cells
Abstract:
Friend erythroleukemic cells (FLC) infected by Polyoma (Py) virus were studied at the electron microscope both during their lytic cycle, which occurs within the first 96 hr after infection, and in the surviving stabilized cells 30 days after infection. The results showed that the Polyoma virus and Friend leukemic virus (FLV) coexist and mature together in the same cell. During the lytic cycle, the Py particles were scattered in the nucleoplasm, and sometimes they were also found aggregated into crystals. Instead crystalline aggregates of Py particles were always present in the few surviving virus-carrying cells 30 days after infection. A possible interpretation could be that the crystal aggregation serves to maintain the viruses in a latency that allows the survival of the host cells.
Insights
Polyoma virus and Friend leukemic virus (FLV) coexist and mature within the same Friend erythroleukemic cells (FLC). Crystal aggregation of Polyoma virus may enable latency and host cell survival.
Area of Science:
- Virology
- Cell Biology
- Electron Microscopy
Background:
- Friend erythroleukemic cells (FLC) are susceptible to viral infections.
- Understanding viral coexistence and latency is crucial for cell survival studies.
Purpose of the Study:
- To investigate the coexistence and maturation of Polyoma virus (Py) and Friend leukemic virus (FLV) in FLC.
- To examine the ultrastructural changes of Py virus during lytic and persistent infection phases.
Main Methods:
- Electron microscopy was used to study FLC infected with Py virus.
- Observation occurred during the lytic cycle (96 hr post-infection) and in stabilized cells (30 days post-infection).
Main Results:
- Polyoma virus and Friend leukemic virus were found to coexist and mature within the same FLC.
- During the lytic cycle, Py particles were scattered or formed crystals in the nucleoplasm.
- Persistent infection showed consistent crystalline aggregates of Py particles in surviving cells.
Conclusions:
- Crystalline aggregation of Polyoma virus particles may play a role in maintaining viral latency.
- This latency mechanism could be essential for the survival of virus-carrying host cells.