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Inhibition of apoptosis by Marek's disease viruses
1Wistar Institute, Philadelphia, PA 19104, USA. ewert@wista.wistar.upenn.edu
Acta Virologica
|March 4, 2000
Summary
Marek's disease virus (MDV) strains can increase lymphoid leukosis by blocking apoptosis. Specific MDV strains, like SB-1, inhibit programmed cell death, promoting survival of cancer-prone B cells.
Area of Science:
- Virology
- Immunology
- Oncology
Background:
- Marek's disease virus (MDV) is a herpesvirus known to enhance lymphoid leukosis development.
- Lymphoid leukosis in poultry can be induced by avian leukosis virus (ALV) or reticuloendotheliosis virus.
Purpose of the Study:
- To investigate the correlation between MDV strains' ability to augment lymphoid leukosis and their capacity to inhibit apoptosis.
- To determine if specific MDV strains provide a survival advantage to B cells with deregulated myc proto-oncogene.
Main Methods:
- Infection of ALV-transformed B cell line DT40 with different MDV strains: MDV-1 (R2/23), MDV-2 (SB1), and MDV-3 (HVT).
- Assessment of apoptosis frequency in normal and infected DT40 cells cultured in serum-reduced medium.
Main Results:
- Normal DT40 cells and those infected with MDV-1 (R2/23) showed high rates of apoptosis.
- DT40 cells infected with MDV-2 (SB1) and MDV-3 (HVT) exhibited significantly reduced apoptosis.
- MDV-2 (SB1) strain persisted in ALV-infected cells, suggesting a role in augmenting lymphoid leukosis.
Conclusions:
- MDV strains differ in their ability to block apoptosis.
- Inhibition of apoptosis by persistent MDV strains like SB-1 may augment lymphoid leukosis by promoting survival of B cells with oncogenic mutations.
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