Bovine Leukemia Virus-Induced Lymphocytosis and Increased Cell Survival Mainly Involve the CD11b+B-Lymphocyte Subset in Sheep
1998
Chevallier, Nathalie | Berthelemy, Madeleine | Le Rhun, Danielle | Laine, V. | Lévy, Daniel | Schwartz-Cornil, Isabelle | Lainé, Véronique | Université Grenoble Alpes - UFR Pharmacie (UGA UFRP) ; Université Grenoble Alpes [2016-2019] (UGA [2016-2019]) | Unité mixte de recherche biologie moléculaire et immunologie parasitaires et fongiques ; Agence Française de Sécurité Sanitaire des Aliments (AFSSA)-École nationale vétérinaire d'Alfort (ENVA)-Institut National de la Recherche Agronomique (INRA)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12) | Chercheur indépendant | Mount Sinai Hospital [Toronto, Canada] (MSH)
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Afficher plus [+] Moins [-]anglais. 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.
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