The immunopathogenesis of equine infectious anemia virus

Sellon, Debra C.; Fuller, Frederick J.; McGuire, Travis C.

doi:10.1016/0168-1702(94)90038-8

Cited by 96 publications

(77 citation statements)

References 130 publications

(191 reference statements)

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“…2A). It has been shown that the in vivo tropism of EIAV is restricted to cells of the monocytemacrophage lineage (76,77). Therefore, equine macrophagederived RNA was examined by RT-PCR using eqA3-specific primers.…”

Section: Resultsmentioning

confidence: 99%

Restriction of Equine Infectious Anemia Virus by Equine APOBEC3 Cytidine Deaminases

Zielonka

Bravo²,

Marino

et al. 2009

J Virol

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The mammalian APOBEC3 (A3) proteins comprise a multigene family of cytidine deaminases that act as potent inhibitors of retroviruses and retrotransposons. The A3 locus on the chromosome 28 of the horse genome contains multiple A3 genes: two copies of A3Z1, five copies of A3Z2, and a single copy of A3Z3, indicating a complex evolution of multiple gene duplications. We have cloned and analyzed for expression the different equine A3 genes and examined as well the subcellular distribution of the corresponding proteins. Additionally, we have tested the functional antiretroviral activity of the equine and of several of the human and nonprimate A3 proteins against the Equine infectious anemia virus (EIAV), the Simian immunodeficiency virus (SIV), and the Adeno-associated virus type 2 (AAV-2). Hematopoietic cells of horses express at least five different A3s: A3Z1b, A3Z2a-Z2b, A3Z2c-Z2d, A3Z2e, and A3Z3, whereas circulating macrophages, the natural target of EIAV, express only part of the A3 repertoire. The five A3Z2 tandem copies arose after three consecutive, recent duplication events in the horse lineage, after the split between Equidae and Carnivora. The duplicated genes show different antiviral activities against different viruses: equine A3Z3 and A3Z2c-Z2d are potent inhibitors of EIAV while equine A3Z1b, A3Z2a-Z2b, A3Z2e showed only weak anti-EIAV activity. Equine A3Z1b and A3Z3 restricted AAV and all equine A3s, except A3Z1b, inhibited SIV. We hypothesize that the horse A3 genes are undergoing a process of subfunctionalization in their respective viral specificities, which might provide the evolutionary advantage for keeping five copies of the original gene.The Equine infectious anemia virus (EIAV) (family Retroviridae, genus Lentivirus) infects equids almost worldwide, causing a persistent infection characterized by recurring viremia, fever, thrombocytopenia, and wasting symptoms (40). EIAV infections are used as a model for natural immunologic control of lentivirus replication and virus persistence and as a test system to improve vaccines against lentiviruses (10,40,41,82). In vivo EIAV replicates predominantly in macrophages (77). Interaction with the equine lentiviral receptor 1 (ELR1) has been demonstrated to be responsible for EIAV internalization (96). There have been no reported cases of EIAV infections in humans, suggesting that it is an intrinsically safe virus and of interest for use in a clinical setting. Therefore, EIAV-based lentiviral vectors for human gene therapy were recently developed (1, 67, 68).In the last few years, two cellular proteins that inhibit many different retroviruses have been characterized: tripartite motif protein 5 alpha (TRIM5␣) and apolipoprotein B mRNAediting enzyme-catalytic polypeptide 3 (APOBEC3 [A3]) (for a review, see reference 92). With respect to TRIM5␣ proteins, both human and nonhuman primate TRIM5␣ orthologues can restrict infection by EIAV (26,72). The activity of equine TRIM5␣ on EIAV infection, however, has not been described so far. With respect to A3 proteins...

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Section: Resultsmentioning

confidence: 99%

Restriction of Equine Infectious Anemia Virus by Equine APOBEC3 Cytidine Deaminases

Zielonka

Bravo²,

Marino

et al. 2009

J Virol

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“…3). The sequences of clinical events, establishment of immune response and virus evolution have been well documented in horses and ponies (Equus caballus) [54,55,83,124,155]. Clinical, serological and virological responses after experimental infection of donkeys (Equus asinus) and detection of virus and description of the disease in mules (Equus caballus × Equus asinus) have been reported [30,161].…”

Section: Eia a Cyclic Diseasementioning

confidence: 99%

Equine Infectious Anemia Virus (EIAV): what has HIV?s country cousin got to tell us?

2004

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-Equine Infectious Anemia Virus (EIAV) is a lentivirus, of the Retrovirus family, with an almost worldwide distribution, infecting equids. It causes a persistent infection characterized by recurring febrile episodes associating viremia, fever, thrombocytopenia, and wasting symptoms. The disease is experimentally reproducible by inoculation of Shetland ponies or horses with EIAV pathogenic strains. Among lentiviruses, EIAV is unique in that, despite a rapid virus replication and antigenic variation, most animals progress from a chronic stage characterized by recurring peaks of viremia and fever to an asymptomatic stage of infection. The inapparent carriers remain infective for life, as demonstrated by experimental transfer of blood to naive animals. The understanding of the correlates of this immune control is of great interest in defining vaccine strategies. Research on EIAV, this "country cousin" of HIV (Human Immunodeficiency Virus), over the last five decades has produced some interesting results on natural immunological control of lentivirus replication and disease and on the nature and role of virus variation in persistence and pathogenesis. These studies are of interest in the context of HIV and efforts to develop a vaccine. This review will focus on some of the most recent results. equine infectious anemia virus / lentivirus / equids / vaccine / viral evolution

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“…This virus is distinct from other lentiviruses such as visna virus or human immunodeficiency virus type 1 (HIV-1) which cause slow progressive courses of disease Sellon et al, 1994). Thus, EIAV may provide an ideal dynamic system for investigating mechanisms of lentivirus persistence and pathogenesis.…”

Section: Introductionmentioning

confidence: 99%

Insertions, duplications and substitutions in restricted gp90 regions of equine infectious anaemia virus during febrile episodes in an experimentally infected horse.

Zheng

Nakaya

Sentsui

et al. 1997

Journal of General Virology

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The immunopathogenesis of equine infectious anemia virus

Cited by 96 publications

References 130 publications

Restriction of Equine Infectious Anemia Virus by Equine APOBEC3 Cytidine Deaminases

Restriction of Equine Infectious Anemia Virus by Equine APOBEC3 Cytidine Deaminases

Equine Infectious Anemia Virus (EIAV): what has HIV?s country cousin got to tell us?

Insertions, duplications and substitutions in restricted gp90 regions of equine infectious anaemia virus during febrile episodes in an experimentally infected horse.

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