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J Virol, May 1998, p. 4413-4420, Vol. 72, No. 5
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Bovine Leukemia Virus-Induced Lymphocytosis and Increased Cell Survival Mainly Involve the CD11b+ B-Lymphocyte Subset in Sheep

Nathalie Chevallier, Madeleine Berthelemy, Danielle Le Rhun, Véronique Lainé, Daniel Levy, and Isabelle Schwartz-Cornil*

URA INRA-DGER d'Immunopathologie Cellulaire et Moléculaire, Ecole Nationale Vétérinaire d'Alfort, 94704 Maisons-Alfort Cedex, France

Received 7 November 1997/Accepted 30 January 1998

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.


* Corresponding author. Mailing address: URA INRA IPCM, ENVA, 7 Avenue du Général de Gaulle, 94704 Maisons-Alfort Cedex, France. Phone: 33 1 43 96 70 75. Fax: 33 1 43 96 71 25. E-mail: schwartz{at}jouy.inra.fr.


J Virol, May 1998, p. 4413-4420, Vol. 72, No. 5
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.



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