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Pathobiology of Bovine Leukemia Virus I Schwartz, D Lévy

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Pathobiology of Bovine Leukemia Virus I Schwartz, D Lévy Pathobiology of bovine leukemia virus I Schwartz, D Lévy To cite this version: I Schwartz, D Lévy. Pathobiology of bovine leukemia virus. Veterinary Research, BioMed Central, 1994, 25 (6), pp.521-536. hal-00902257 HAL Id: hal-00902257 https://hal.archives-ouvertes.fr/hal-00902257 Submitted on 1 Jan 1994 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Review article Pathobiology of bovine leukemia virus I Schwartz D Lévy URA-INRA d’Immuno-Pathologie Cellulaire et Moléculaire, École Nationale Vétérinaire dAlfort, 7, avenue du Général-de-Gaulle, 94704 Maisons-Alfort cedex, France (Received 16 March 1994; accepted 25 July 1994) Summary ― Bovine leukemia virus (BLV) is a retrovirus similar to the human T-cell leukemia virus (HTLV). Most BLV infected animals (70%) develop a B-cell lymphoproliferative syndrome with altered productive traits and 1 to 5% die with B-cell lymphosarcomas. Although BLV infection is worid-wide, west- ern European countries have almost eradicated it by slaughtering the seropositive animals. BLV infec- tion remains endemic in many countries including the United States and prophylactic strategies involv- ing recombinant vaccine vectors, genetically modified BLV and transgenic animals resistant to the infection are under study. BLV / animal models / leukosis Résumé ― Pathobiologie du virus de la leucose bovine enzootique. Le virus de la leucose bovine enzootique (BL V) est un rétrovirus semblable au virus leucémogène humain HTLV La plupart (70%) des bovins infectés par ce virus développent une prolifération lymphocytaire B accompagnée d’une dimi- nution des performances zootechniques, et 1 à 5% des animaux meurent de lymphosarcome B. Bien’ que l’infection par le BL V soit mondialement répandue, les nations de l’Europe occidentale l’ont pra- tiquement éradiquée par abattage systématique des animaux séro-positifs. L’infection par le BLV reste cependant endémique dans de nombreux pays, comme les États-Unis. Des stratégies de pro- phylaxie faisant appel à la vaccination avec des vecteurs vaccine recombinants pour la protéine d’enveloppe, ! des provirus BL V génétiquement modifiés et à des animaux transgéniques résistants sont en cours d’étude. BLVlmodèles animauxlleucémie * Correspondence and reprints INTRODUCTION and molecular knowledge about BLV, and to stress the biological aspects which pro- vide us with an and model The bovine leukemia virus is a cat- original powerful (BLV) for and retroviral diseases. tle retrovirus responsible for bovine enzootic studying fighting leukemia. Its genetic structure, sequence and many similarities pathogenicity present HISTORICAL BACKGROUND to those of the human T-cell leukemia viruses (HTLV-1 and 2). Seventy percent of the infected cattle present a chronic The first reported case of bovine leukemia increase in the number of circulating B lym- was described in 1871 in the Klaipeda area, phocytes, which can lead to a haematolog- Lithuania, and mentioned a cow with super- ical status called persistent lymphocytosis, ficial lymph node hypertrophy and and 1 to 5% of the infected cattle develop a splenomegaly (Burny et al, 1980). There- B-cell lymphosarcoma (Burny et al, 1988). after other cases were reported, indicating’ BLV infection involves a large number of that the disease was propagating west and cattle around the world and the prevalence it eventually reached the USA. In 1917, Ken- is high on the American continent, in Aus- neth showed that the disease was medi- tralia, Africa, and Asia. As herd contamina- ated by a contagious agent (Burny et al, tion follows the introduction of an infected 1980). In 1969, Miller et al discovered that animal, many European countries have lymphocytes of cows with persistent lym- decided to eradicate the infection by apply- phocytosis produced viral particles that were ing strict sanitary measures. Nowadays lym- visible by electron microscopy after in vitro phosarcoma cases are rarely found in most culture (Miller et al, 1969). In 1976, western European countries. Kettmann et al showed that BLV particles Except for the rare lymphosarcoma are RNA exogenous viruses and carry a lesions, the impact of BLV on bovine health RNA reverse transcriptase complex; this and productivity is not well known and still finding allowed the classification of BLV raises many questions. Our purpose here is amongst the oncogenic retroviruses to review the epidemiological, pathological (Kettmann et al, 1976). BLV PATHOGENICITY lymphocyte population of a different lineage from the CD5- B-cells that could be involved in the synthesis of autoantibodies BLV induces a persistent and chronic infec- et This of tion that affects essentially the B lympho- (Hayakawa al, 1985). type lym- is also found in chronic cyte population (Kettmann et al, 1980; Levy phocyte lymphoid leukemia in humans la Hera et al, 1988). et al, 1987). The infection can be transmit- (De Are CD5+ the ted by the cellular components of infected B-lymphocytes preferential for BLV infection? fluorescence bovine blood, by infected cultured cells, or by target Using we BLV free viral particles produced in cell culture activated cell sorting, showed that is found in CD8+ (Burny et al, 1980). Viraemia is only T-lymphocytes, monocytes, detectable during the first 2 weeks of infec- granulocytes, and mostly in B-lymphocytes, tion (Portetelle et al, 1978). Thereafter the with no preference for the CD5+ B-cell pop- The expression of viral antigens is difficult to evi- ulation (Schwartz et al, 1994). param- eters in the of the CD5+ dence but it can sometimes be detected in involved sensitivity to the the intrafollicular and margin zones of lymph B-lymphocytes lymphoproliferative nodes using immunocytochemistry (Heeney potential of BLV remain to be determined. et al, 1992). Cattle develop a serological The ultimate and rare expression of BLV response to capsid and envelope proteins infection is the emergence of a multicentric 2-8 weeks after inoculation (Burny et al, lymphosarcoma that occurs 1-8 years after 1980). These antibodies are lifelong and infection, in about 1-5% of the animals show important level variations that proba- (Burny et al, 1980; Lewin, 1989). Two-thirds bly relate to the physiological and immune of the animals with tumors have had a per- status of the animal. Antibodies to viral reg- sistent lymphocytosis (Burny et al, 1980). ulatory proteins (the Tax and Rex proteins) The tumors may affect 1 or several super- can also be detected in about 20% of ficial and/or deep lymph nodes (Burny et al, infected cattle (Powers et al, 1991). 1980). In a single animal, tumors are mostly In the years following infection, 70% of monoclonal for BLV integration and the virus infected animals show an increase in the does not seem to display preferential inte- B/T lymphocyte ratio in the blood, with a gration sites among tumors from different seemingly normal total number of lympho- animals (Kettmann etal, 1983). According to cytes (4 000 to 10 000/ mm3) (Lewin, 1989). some authors, the tumor cells are pre-B- Among these animals, half develop a per- lymphocytes that are characterized by the sistent lymphocytosis, which corresponds lack of expression of the immunoglobulin to a stable increase in the number of circu- light chain (Van den Broecke et al, 1988); for lating lymphocytes, sometimes reaching up others, they are mature B-lymphocytes to 100 000/mm3 (Lewin, 1989). The inte- showing an isotypic commutation in the gration of the BLV genome is found in 30% immunoglobulin gene (Heeney and Valli, of the circulating lymphocytes and concerns 1990). Most often, the CD5 marker is many clones of lymphocytes (Kettmann et expressed on the tumor cells (Depelchin et al, 1980). The expansion of the lymphocyte al, 1989; Letesson et al, 1991 ). This tumoral population results from the polyclonal pro- form of BLV only affects adult cattle that are liferation of mature B lymphocytes which over 2 years of age, with an incidence peak are cytologically and karyotypically normal around the age of 5-8 years (Lewin, 1989). (Grimaldi ef al, 1983). Most of these lym- This has to be distinguished from the bovine phocytes carry the CDS, CDllb and CD11cc leukemia sporadic cases that affect animals markers (Letesson etal, 1991). In mice, it under 1 year of age and that are not asso- seems that the CD5+ B-cells constitute a B- ciated with BLV infection. BLV TRANSMISSION viral load at the time of infection (Mammer- ickx et al, 1988). It seems that the higher sensitivity of sheep to BLV pathogenicity is Natural transmission related to a higher permissiveness of ovine cells to viral replication (Burny et al, 1980). Ovine intraspecies transmission is extremely In natural conditions, zebus, buf- only cattle, rare in natural conditions and are cases of in falos and have been found to be capybaras utero or accidental transmission et al, infected (Bumy (Burny ef al, 1980). 1980). The virus is transmitted infected by lym- Goats are sensitive to BLV infection, but About 1 500 from phocytes. lymphocytes only 2 out of 24 infected animals developed a cow with persistent lymphocytosis (0.1 !I lymphoid tumors in 10 years (Burny et al, of are sufficient to infect another ani- blood) 1980). mal (Mammerickx et al, 1988). Most of the BLV infection in rabbits is an time, contamination is iatrogenic and occurs interesting model as rabbits an when the animals are manipulated without experimental develop the respect of hygiene recommendations immunodeficiency syndrome 45-763 d after infection et al, After for injections, horning, tattooing or rectal (Altanerova 1989).
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