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Bovine Immunodeficiency Virus: Facts and Questions C Belloc, B Polack, I Schwartz-Cornil, J Brownlie, D Lévy

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Bovine Immunodeficiency Virus: Facts and Questions C Belloc, B Polack, I Schwartz-Cornil, J Brownlie, D Lévy Bovine immunodeficiency virus: facts and questions C Belloc, B Polack, I Schwartz-Cornil, J Brownlie, D Lévy To cite this version: C Belloc, B Polack, I Schwartz-Cornil, J Brownlie, D Lévy. Bovine immunodeficiency virus: facts and questions. Veterinary Research, BioMed Central, 1996, 27 (4-5), pp.395-402. hal-00902431 HAL Id: hal-00902431 https://hal.archives-ouvertes.fr/hal-00902431 Submitted on 1 Jan 1996 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 Bovine immunodeficiency virus: facts and questions C Belloc B Polack I Schwartz-Cornil J Brownlie D Lévy 1 Unité de recherche associée d’immunopathologie cellulaire et moléculaire, Inra, École nationale vétérinaire dAlfort, 7, avenue du Général-de-Gaulle, 94704 Maisons-Alfort cedex, France; 2 Royal Veterinary College, London, UK (Received 28 November 1995; accepted 29 March 1996) Summary ― Bovine immunodeficiency virus (BIV) is a lentivirus whose serologic prevalence is worldwide. Little is known about its impact on animal health status, pathogenesis and mode of transmission. Understanding BIV biology implies isolation of new viral strains and long-term studies on experimentally-infected cows and surrogate hosts such as rabbits. bovine immunodeficiency virus / cattle / review / lentivirus Résumé ― Le virus de l’immunodéficience bovine : faits et interrogations. Le virus de l’immunodéficience bovine (BIV) est un lentivirus dont la séroprévalence est mondiale. Actuellement, on connaît mal ses conséquences en matière de santé animale ainsi que son pouvoir pathogène ou ses modes de transmission. Afin de répondre aux différentes questions concernant le BIV, il est nécessaire d’isoler de nouvelles souches virales et de réaliser un suivi prolongé d’animaux infectés expérimentalement. virus de l’immunodéficience bo vine l bovin / revue générale l lentivirus .!--- * Correspondence and reprints INTRODUCTION signs suggesting bovine leukosis (Malmquist et al, 1969; Van der Maaten et al, 1972). It was first designated ’bovine visna-like virus’ The bovine immunodeficiency virus (BIV) and remained unstudied until HIV was dis- is a lentivirus and one of the three morpho- covered, which generated renewed interest biologically and genetically distinct logically, in the study of animal lentiviruses. BIV was syncytium-inducing retroviruses infecting further characterized using molecular biology bovines. Retroviruses are a of RNA family techniques and two proviral infectious clones viruses that are for both man pathogenic were sequenced: BIV R-29 106 and BIV R- and animals. Chronologically, BIV was the 29 127 (Gonda et al, 1987; Garvey et al, third animal lentivirus to be discovered 1990). To date, all serologic information infec- among a group of eight, after equine relating to the presence of a BIV infection tious anemia virus (Vallée and Carr6, 1904) has been obtained using the original R-29 and ovine visna-maedi virus (Sigurdss6n et isolate as the antigen. Only recently have al, 1960). However the role of BIV as a new field isolates become available in the potential pathogen as well as its actual USA (Suarez et al, 1993). in remain prevalence, especially Europe, A new bovine lentivirus, the Jembrana unknown. Our here is to totally purpose disease virus (JDV), associated with a and review the epidemiological, pathological severe acute syndrome in Bali cattle (Bos molecular knowledge concerning BIV. javanicus), has been found to be both anti- genically and genetically closely related to BIV (Kertayadnya et al, 1993; Chadwick et HISTORICAL BACKGROUND al, 1995). BIV was discovered in 1969 during the inten- PREVALENCE OF BIV INFECTION sive search for the causative agent of enzootic bovine leukosis. A virus with the morphology of a lentivirus was isolated from Serologic evidence for BIV infection has R-29, a pregnant dairy cow with clinical been reported in many countries around the world following a non-uniform distribution. infectious agents. Nevertheless, cow R-29 The prevalence of BIV infection is 4% in the had evidence of lymphocytosis, lym- southern and southwestern states of the phadenopathy, central nervous system USA (Black, 1989) and average frequen- lesions and emaciation (Van der Maaten et al, cies of 64% and 40% have been reported in 1972). Moreover, hematological changes, the Louisiana area within dairy and beef lymphadenopathy with follicular hyperplasia, herds respectively. In Canada and the skin lesions unresponsive to treatment and Netherlands, the prevalence is 5.5% and meningoencephalitis have been found in nat- 1.4% (McNab et al, 1994; Horzinek et ai, urally- and experimentally-infected cattle 1991 ). In France, we have found that 4% (Braun et al, 1988; Martin et al, 1991; Car- of selected cattle tested positive for BIV penter et al, 1992; Onuma et al, 1992; Flam- (Polack et al, 1996). We also observed a ing et al, 1993; Gonda et al, 1994; Rovid et al, higher prevalence in dairy than in beef herds 1995). In these animals, the virus is tran- which may be the result of herd manage- scriptionally active and can be isolated for ment practices and of the extended pro- many years after infection (Brownlie et al, ductive life of dairy relative to beef cattle. 1994; Baron et al, 1995). Jembrana disease Seropositive cattle have also been detected virus is highly pathogenic in B javanicus in Great Britain (Brownlie et al, 1994; Howie whereas it does not induce any disease in B et al, 1994), Switzerland, Australia (Forman taurus. The parameters determining this dif- et al, 1992), Costa-Rica, Venezuela (in ferential pathology remain to be discovered. Gonda et al, 1994) and Brazil (unpublished Obviously, the BIV strains, bovine breed and personal results). Since the European sera the environment are factors that may influ- react weakly with the R-29 antigen, local ence susceptibility to BIV disease. Long-term isolates may be antigenically different from studies are thus necessary to observe BIV the American ones (Horzinek et al, 1991; pathogenicity since current opinions are Polack et al, 1996). Consequently, wild-type based on a limited number of short-term isolates are also needed in order to develop experimental studies. Finally, lentiviruses specific detection assays based on anti- exhibit variable virulence according to iso- bodies or nucleic acids. lates. Isolation of new BIV variants is neces- sary in order to appreciate its pathogenesis. CLINICAL AND PATHOLOGICAL FEATURES HOST TROPISM Lentivi ruses are responsible for a persistent In vivo, bovines are the major naturally- lifelong infection despite inducing a strong infected animals. Antibodies against BIV immune response. The onset of the disease have been reported in sheep and goats, is preceded by a several-year incubation however, without successful isolation of the period. It affects multiple organs and is char- virus or evidence of viral DNA (Whestone acterized by progressive debilitation, which, et al, 1991; Jacobs et al, 1994). Rabbits in the case of HIV, leads to death. The sig- experimentally-infected with BIV exhibit alter- nificance of BIV infection on the health status ations in their immune response (Onuma et of field herds has not been clearly estab- al, 1990; Pifat et al, 1992; Van der Maaten lished due to the high turnover rate of pro- and Whestone, 1992; Archambault et al, duction animals. It is not known whether BIV 1993; Hirai et al, 1994). The virus can be induces a specific syndrome or whether it isolated from the peripheral blood mononu- renders animals more susceptible to other clear cells, spleen, lymph nodes and brain throughout the life time of the infected ani- VIRUS BIOLOGY mals. In transgenic mice, BIV induces a meningoencephalitis associated with an BIV infection early 50% mortality (Gonda et al, 1994). cycle Such neurological syndromes have been reported with HIV-1 transgenic mice BIV particles consist of two positive-sense (Leonard et al, 1988). single-stranded viral RNAs and have a struc- tural capsid which envelops proteins. Mice, rats and guinea pigs are not sus- ceptible to BIV infection (Gonda, 1992). BIV is an exogenous retrovirus with a replication cycle similar to that of other lentiviruses. Free virus particles attach to CELL TROPISM specific surface receptors and penetrate into the cell. The viral RNA is then released and converted by a viral reverse transcriptase In vitro, BIV is able to infect a broad range of into double-stranded DNA that is integrated adherent and cells suspension originating into the cellular genome, a step that involves from different tissues and different animal a viral integrase. This integrated provirus species (Gonda et al, 1990; Gonda, 1992). remains inactive unless appropriate cellular In fibroblast-like BIV induces a cells, cyto- signals occur. When activated, genomic and effect characterized for- pathic by syncytium subgenomic messages are translated in the mation. Through analogy with other cytoplasm. Viral particle assembly and RNA lentiviruses, the in vivo targets of BIV infec- incorporation occur near the plasma mem- tion are likely to be the immune cells of the brane. Cellular machinery and viral proteins lymphoid and monocyte/macrophage lin- contribute to each step of this process. eages. BIV provirus can be detected by polymerase chain reaction from the periph- eral blood mononuclear cells, spleen, lymph Genomic organization nodes and brain (Pifat et al, 1992; Oberste et al, 1991 However, the cellular receptor The BIV genome (proviral DNA) is 8 960 for BIV has not yet been characterized. nucleotides long and contains the obliga- tory retroviral structural genes gag, pol and envflanked on the 5’ and 3’ termini by long BIV TRANSMISSION terminal repeats (LTR) (fig 1).
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