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Updated: Aug 5, 2026

07:02
Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus (KSHV)
Published on: September 14, 2010
Viral expressions in Reed-Sternberg cells
J G Sinkovics1, F Gonzalez, F Gyorkey
1Cancer Institute, St. Joseph's Hospital, Tampa, Florida 33677.
Leukemia
|January 1, 1992
Summary
Natural hybridoma formation in mice involves lymphoma and plasma cells fusing to produce MLV particles and antibodies. This process may explain the origin and marker heterogeneity of Reticulum Cell Sarcoma (RS) cells.
Area of Science:
- Immunology
- Virology
- Oncology
Background:
- Natural hybridoma formation was first observed in murine systems in 1968-9.
- The #620 to 818 system involves fusion between a mouse leukemia virus (MLV)-producing diploid lymphoma cell and an immune plasma cell.
Purpose of the Study:
- To propose an analogy between the #620 to 818 system and the origin of Reticulum Cell Sarcoma (RS) cells.
- To explain the heterogeneity of RS cell markers through a natural hybridoma model.
Main Methods:
- Observation of natural hybridoma formation in a murine system.
- Analysis of fusion products from MLV-producer lymphoma cells and immune plasma cells.
- Indirect evidence suggesting retroviral infection of mononuclear HD (interdigitating reticulum) cells.
Main Results:
- Fusion product cells exhibited tetraploidy, grew in suspension and as ascites tumors, and produced MLV particles and neutralizing antibodies.
- Retroviral infection of interdigitating reticulum (IR) cells followed by fusion with reactive B and T cells is suggested.
- Fusion products showed hyperdiploidy and marker disarray, with loss of IR markers and gain of B/T cell markers.
Conclusions:
- The natural hybridoma model, involving fusion of IR cells with B and/or T lymphocytes, provides a plausible explanation for the origin and marker heterogeneity of RS cells.
- This model challenges conventional theories that fail to account for the diverse markers observed in RS cells.
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