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Published on: October 14, 2016
Infection of an established mouse cell line with cell-free Rauscher leukemia virus. I. Cytological study with the
1John L. Smith Memorial for Cancer Research, Chas. Pfizer & Company, Inc., Maywood, New Jersey 07607, USA.
Abstract:
Infecting mouse bone marrow cells (JLS-V9) with cell-free Rauscher leukemia virus demonstrated that monolayers of JLS-V9 cells were susceptible to infection with both cell-free plasma and tissue-culture-propagated Rauscher virus. The infected cultures maintained the continuous release of the virus. Cells and concentrated supernatant fluids from infected cells were periodically examined under the electron microscope by thin sectioning and negative staining techniques after inoculation with either mouse plasma or tissue-culture-propagated virus. After adsorption the virus underwent a prolonged eclipse or latent period. Virus budding was initially detected about 10 days after primary infection. These observations were further confirmed by the simultaneous appearance of extracellular virus. The budding process was followed by accelerated virus multiplication which reached maximum production 2-3 weeks later. Before the onset of budding no significant morphologic changes were seen in the infected cells.
Insights
Mouse bone marrow cells infected with Rauscher leukemia virus continuously released the virus after a latent period. Electron microscopy revealed virus budding and multiplication starting around 10 days post-infection.
Area of Science:
- Virology
- Cell Biology
- Oncology
Background:
- Rauscher leukemia virus (RLV) is an oncogenic retrovirus known to cause leukemia in mice.
- Understanding the early stages of RLV infection is crucial for developing antiviral strategies.
Purpose of the Study:
- To investigate the susceptibility of mouse bone marrow cells (JLS-V9) to Rauscher leukemia virus infection.
- To characterize the replication cycle and release of RLV in infected cell cultures.
Main Methods:
- Infection of JLS-V9 cell monolayers with cell-free Rauscher leukemia virus (from plasma or tissue culture).
- Electron microscopy (thin sectioning and negative staining) to examine infected cells and supernatant fluids.
- Monitoring for virus release and morphological changes over time.
Main Results:
- JLS-V9 cells are susceptible to RLV infection, leading to continuous virus release.
- A prolonged eclipse/latent period precedes detectable virus budding, observed around 10 days post-infection.
- Accelerated virus multiplication occurs 2-3 weeks after initial infection, with no significant cell morphology changes before budding.
Conclusions:
- JLS-V9 cells support Rauscher leukemia virus replication and continuous release.
- The early RLV replication cycle in these cells involves a significant latent period followed by budding and multiplication.
