Strains of Marek's disease virus (MDV), a herpesvirus, have been shown to a
ugment the development of lymphoid leukosis induced by retroviruses, the av
ian leukosis virus (ALV) or the reticuloendotheliosis virus. In this study
we explored the possibility that the ability to augment lymphoid leukosis m
ay be correlated with the ability of different strains of MDV to block apop
tosis. Subclones of the ALV-transformed B cell line, DT40, which was free o
f MDV DNA were infected with either R2/23 strain of MDV-1, SB1 strain of MD
V-2, or turkey herpes virus (HVT), a MDV-3. We found that most of the norma
l DT40 cells and DT40 cells infected with the R2/23 became apoptotic when c
ultured in serum-reduced medium. By contrast, the frequency of apoptotic ce
lls was greatly reduced in the DT40-SB1 and DT40-HVT subclones. These findi
ngs suggest that because the SB-1 strain persists in the ALV-infected cells
, it may augment lymphoid leukosis by inhibiting apoptosis and providing a
survival advantage to the B cells which have a deregulated myc proto-oncoge
ne.