Bovine leukemia virus-induced lymphocytosis and increased cell survival mainly involve the CD11b+ B-lymphocyte subset in sheep.
In this study, we show that bovine leukemia virus (BLV)-induced persistent lymphocytosis (PL) results from the in vivo expansion of the CD11b+ B-lymphocyte population. This subset shares phenotypic characteristics 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-infected sheep, the viral load is higher in B-1-like cells and only B-1- and 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- and B-2-like cells, indicating that both cell types support viral replication. Finally, cycloheximide and a protein kinase C inhibitor (H7) that blocks the ex vivo activation of viral expression did not affect the 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 effects and further support the involvement of increased survival in BLV pathogenesis.
Chevallier
N
N
URA INRA-DGER d'Immunopathologie Cellulaire et Moléculaire, Ecole Nationale Vétérinaire d'Alfort, Maisons-Alfort, France.
Berthelemy
M
M
Le Rhun
D
D
Lainé
V
V
Levy
D
D
Schwartz-Cornil
I
I
D000818:Animals; D017209:Apoptosis; D016175:B-Lymphocyte Subsets / Q000276:immunology*; D002417:Cattle; D002470:Cell Survival; D016583:Enzootic Bovine Leukosis / Q000276:immunology* / Q000503:physiopathology / Q000821:virology; D001909:Leukemia Virus, Bovine / Q000276:immunology*; D008218:Lymphocytosis / Q000276:immunology* / Q000503:physiopathology / Q000821:virology; D016177:Macrophage-1 Antigen / Q000276:immunology*; D012756:Sheep; D013997:Time Factors; D019562:Viral Load
D016177:Macrophage-1 Antigen