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Debacq, Christophe; Alcaraz, Maria Teresa Sanchez; Mortreux, Franck; Kerkhofs, Pierre; Kettmann, Richard; Willems, Luc

doi:10.1186/1742-4690-1-31

Cited by 23 publications

(8 citation statements)

References 46 publications

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“…Mutations within the LTR further revealed that the viral promoter contained sub-optimal enhancers ( A GACGTCA, TGACG G CA, TGAC C TCA) that are essential for viral replication. As expected, site directed mutagenesis of the enhancers into consensus cyclic-AMP responsive elements (TGACGTCA) increases promoter efficiency but strongly impairs viral replication [ 28 , 29 ]. The presence of suboptimal enhancers in all BLV and HTLV-1 isolates suggests an evolutionary conserved mechanism that may reduce basal transcription and facilitate the escape from immune response.…”

Section: Reverse Genetics Reveals the Significance Of Viral Sequenmentioning

confidence: 85%

Recent Advances in BLV Research

Barez

Brogniez

Carpentier

et al. 2015

Viruses

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Different animal models have been proposed to investigate the mechanisms of Human T-lymphotropic Virus (HTLV)-induced pathogenesis: rats, transgenic and NOD-SCID/γcnull (NOG) mice, rabbits, squirrel monkeys, baboons and macaques. These systems indeed provide useful information but have intrinsic limitations such as lack of disease relevance, species specificity or inadequate immune response. Another strategy based on a comparative virology approach is to characterize a related pathogen and to speculate on possible shared mechanisms. In this perspective, bovine leukemia virus (BLV), another member of the deltaretrovirus genus, is evolutionary related to HTLV-1. BLV induces lymphoproliferative disorders in ruminants providing useful information on the mechanisms of viral persistence, genetic determinants of pathogenesis and potential novel therapies.

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Section: Reverse Genetics Reveals the Significance Of Viral Sequenmentioning

confidence: 85%

Recent Advances in BLV Research

Barez

Brogniez

Carpentier

et al. 2015

Viruses

Self Cite

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“…This rule applies not only to viruses but to all representatives of all taxonomic kingdoms (Markov, Naimark, 2015). And one of the truly harmful qualities of viruses is not their virulence as such but the immune responses provoked by a (Debacq et al, 2004;Lezin et al, 2009;Agol, 2015). When we assume that BLV does not alter the host complex of the synthesized proteins without introducing anything of "its own" (Kettmann et al, 1980), such a theory looks quite plausible.…”

Section: Discussionmentioning

confidence: 99%

Association of haplotypes for SNPs in the LTR regions of bovine leukemia virus with hematological indices of cattle

et al. 2019

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Molecular typing of BLV samples isolated from Holsteinized Russian Black Pied cattle was carried out, and various cytofluorometric and morphological blood indices were examined. We performed the total count of white blood cells (WBC), lymphocyte (lymf), granulocyte (gran), monocyte (mon), red blood cell (RBC), hemoglobin (HGB), hematocrit (HTC), mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC), red blood cell distribution width (RDW), platelet count (PLT), mean platelet volume (MPV), platelet distribution width (PDW), and platelet crit count (PCT). The LTR-region of BLV was haplotyped. Only viruses of haplotypes I (0.33±0.03) and III (0.67±0.03) of the eight possible were detected. The ratio of hematologically sick, healthy, and suspected carriers of BLV of haplotypes I and II was comparable with the results of other researchers. The numbers of leukocytes, erythrocytes and platelets in the blood of carriers of haplotype III exceeded the corresponding parameters of cattle affected by the virus of haplotype I. It is interesting to note that the difference in the hemolytic status of animals was manifested not only by the concentration of leukocytes as direct immune agents but also by the count of erythrocytes and platelets, which are not directly involved in the immune response. The number of particles of haplotype III of the BLV circulating in the blood of infected individuals exceeded that of the carriers of haplotype I. In this connection, an assumption was made about the evolutionary advantage of the more virulent haplotype III. However, the results of our own research in conjunction with the data of other scientists indicate that the high virulence of individual virus strains is a consequence of the tendency to implement the maximum possible intensity of the synthesis of virus particles but not of the high damaging effect alone. It is shown that high lethality is evolutionarily disadvantageous for viruses, since the extinction of the carrier as a biological species is fraught with the disappearance of the virus itself.

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“…Primary infection of sheep S1, S2, and S3 correlated with a transient accumulation of B lymphocytes peaking at the seroconversion period, i.e., the time at which BLV-specific neutralizing antibodies appear in the serum (arrow in Fig. 3A) (31). Active viral replication also occurs during this period, as revealed by an increase in the proviral loads (Fig.…”

Section: Valproate Is Proapoptotic and Increases The Level Of Blv Expmentioning

confidence: 91%