BOVINE LEUKEMIA VIRUS-INDUCED LYMPHOCYTOSIS AND INCREASED CELL-SURVIVAL MAINLY INVOLVE THE CD11B(-LYMPHOCYTE SUBSET IN SHEEP() B)

In this study, we show that bovine leukemia virus (BLV)-induced persis tent lymphocytosis (PL) results from the in vivo expansion of the CD11 b(+) B-lymphocyte population. This subset shares phenotypic characteri stics with murine and human B-1 cells. BLV interactions with the sheep B-1-like subset were explored. We found that B-1- and B-2-like cells are initially infected to similar extents. However, in long-term-infec ted sheep, the viral load is higher in B-1-like cells and only B-1- an d not B-2-like cells show increased ex vivo survival compared to that in uninfected sheep. Ex vivo viral expression was found in both B-1- a nd B-2-like cells, indicating that both cell types support viral repli cation, Finally, cycloheximide and a protein kinase C inhibitor (H7) t hat blocks the ex vivo activation of viral expression did not affect t he increased survival in B-1-like cells, suggesting that resistance to apoptosis is acquired in vivo. Collectively, these results indicate a peculiar susceptibility of sheep B-1-like cells to BLV transforming e ffects and further support the involvement of increased survival in BL V pathogenesis.