Document Detail

Cell dynamics and immune response to BLV infection: a unifying model.
MedLine Citation:
PMID:  17127399     Owner:  NLM     Status:  MEDLINE    
Bovine Leukemia virus (BLV) is the natural etiological agent of a lymphoproliferative disease in cattle. BLV can also be transmitted experimentally to a related ruminant species, sheep, in which the pathogenesis is more acute. Although both susceptible species develop a strong anti-viral immune response, the virus persists indefinitely throughout life, apparently at a transcriptionally silent stage, at least in a proportion of infected cells. Soon after infection, these humoral and cytotoxic activities very efficiently abolish the viral replicative cycle, permitting only mitotic expansion of provirus-carrying cells. Short term cultures of these infected cells initially indicated that viral expression protects against spontaneous apoptosis, suggesting that leukemia is a process of accumulation of long-lived cells. This conclusion was recently reconsidered following in vivo dynamic studies based on perfusions of nucleoside (bromodeoxyuridine) or fluorescent protein markers (CFSE). In sheep, the turnover rate of infected cells is increased, suggesting that a permanent clearance process is exerted by the immune system. Lymphocyte trafficking from and to the secondary lymphoid organs is a key component in the maintenance of cell homeostasis. The net outcome of the immune selective pressure is that only cells in which the virus is transcriptionally silenced survive and accumulate, ultimately leading to lymphocytosis. Activation of viral and/or cellular expression in this silent reservoir with deacetylase inhibitors causes the collapse of the proviral loads. In other words, modulation of viral expression appears to be curative in lymphocytic sheep, an approach that might also be efficient in patients infected with the related Human T-lymphotropic virus type 1. In summary, a dynamic interplay between BLV and the host immune response modulates a complex equilibrium between (i) viral expression driving (or) favoring proliferation and (ii) viral silencing preventing apoptosis. As conclusion, we propose a hypothetical model unifying all these mechanisms.
Arnaud Florins; Nicolas Gillet; Becca Asquith; Mathieu Boxus; Catherine Burteau; Jean-Claude Twizere; Patrice Urbain; Fabian Vandermeers; Christophe Debacq; Maria Teresa Sanchez-Alcaraz; Isabelle Schwartz-Cornil; Pierre Kerkhofs; Genèvieve Jean; Andre Théwis; Jack Hay; Franck Mortreux; Eric Wattel; Michal Reichert; Arsène Burny; Richard Kettmann; Charles Bangham; Luc Willems
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2007-01-01
Journal Detail:
Title:  Frontiers in bioscience : a journal and virtual library     Volume:  12     ISSN:  1093-4715     ISO Abbreviation:  Front. Biosci.     Publication Date:  2007  
Date Detail:
Created Date:  2006-11-27     Completed Date:  2007-08-23     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9709506     Medline TA:  Front Biosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1520-31     Citation Subset:  IM    
Molecular and Cellular biology, FNRS-FUSAG, Gembloux, Belgium.
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MeSH Terms
Antibody Formation
Enzootic Bovine Leukosis / drug therapy,  immunology*,  virology*
Leukemia Virus, Bovine / genetics,  pathogenicity*,  physiology
Models, Immunological*
Sheep Diseases / virology
T-Lymphocytes, Cytotoxic / immunology
Transcription, Genetic
Virus Replication

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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