par Burny, Arsène 
;Kettmann, Richard ;Cleuter, Yvette ;Marbaix, Gérard ;Portetelle, Daniel ;Van Den Broeke, Anne ;Willems, Lucas ;Thomas, René ;Mammerickx, Marc
Référence Advances in Veterinary Science and Comparative Medicine, 32, page (149-170)
Publication Publié, 1988
;Kettmann, Richard ;Cleuter, Yvette ;Marbaix, Gérard ;Portetelle, Daniel ;Van Den Broeke, Anne ;Willems, Lucas ;Thomas, René ;Mammerickx, MarcRéférence Advances in Veterinary Science and Comparative Medicine, 32, page (149-170)
Publication Publié, 1988
Article révisé par les pairs
| Résumé : | Bovine leukemia virus is the etiological agent of a chronic lymphatic leukemia/lymphoma in cows, sheep, and goats. Structurally and functionally, BLV is a relative of the human T lymphotropic viruses (HTLV-I and HTLV-II). HTLV-I induces in humans a T-cell leukemia, and its type II counterpart has been found in dermatopathic lymphadenopathy, hairy T-cell leukemia, and prolymphocytic leukemia cases. BLV, HTLV-I, and HTLV-II show clearcut sequence homologies. The pathology of the BLV-induced disease, most notably, the absence of chronic viremia, a long latency period, and a lack of preferred proviral integration sites in tumors, is similar to that of adult T-cell leukemia/ lymphoma induced by HTLV-I. The most striking feature of the three naturally transmitted leukemia viruses is the X region located beween the env gene and the LTR sequence. The X region contains several overlapping long open reading frames. One of them designated XBL-I encodes a transactivator function capable of increasing the level of gene expression directed by BLV-LTR and most probably involved in genetic instability of BLV-infected cells of the B-cell lineage. The genetic instability puts the cell into a context of fragility and ready to move along a number of stages towards full malignancy. © 1988, Elsevier B.V. All rights reserved. |
