Constitutive and visna virus induced expression of class I and II major histocompatibility complex antigens in the central nervous system of sheep and their role in the pathogenesis of visna lesions

Bergsteinsdóttir, Kristín; Árnadóttir, Steinunn; Torsteinsdóttir, Sigurbjörg; Agnarsdóttir, Gudrún; Andrésdóttir, Valgerður; Pétursson, Gudmundur; Georgsson, Guðmundur

doi:10.1046/j.1365-2990.1998.00100.x

Cited by 11 publications

(9 citation statements)

References 38 publications

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“…Expression of MHC was detected on cultured ovine microglial cells, with MHC-class I staining more prominent than MHC-class II staining. This is consistent with previous in vivo studies in which ovine parenchymal microglial cells were shown to express both MHCclass I and class II molecules (Torsteinsdottir et al, 1994;Bergsteinsdottir et al, 1998).…”

Section: Discussionsupporting

confidence: 93%

Phenotypic characterisation and infection of ovine microglial cells with Maedi-Visna Virus

Ebrahimi¹,

Allsopp²,

Fazakerley³

et al. 2000

J Neurovirol

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Maedi-Visna Virus (MVV) infection of the central nervous system (CNS) results in pathological changes, the mechanisms of which are poorly understood. MVV preferentially infects cell of the monocyte/macrophage lineage in vivo. The neuroparenchymal microglial cells are the resident tissue macrophages in the CNS and therefore likely targets for MVV infection. However, no information is currently available on the susceptibility of these cells to MVV infection or their contribution to neuropathological changes as a result of MVV infection. Highly enriched primary ovine microglial cell cultures were set up from brain tissues of lambs. These cells were amoeboid or bipolar with spikes, a morphology consistent with microglial cells of other species, and stained positive for CD1, CD11a, CD11c, CD14, MHC-class I, MHC-class II, and b-N-acetyl galactose, but not with markers of astrocytes or oligodendrocytes. These sheep microglial cells were permissive for MVV infection. Productive MVV infection resulted in selective transcriptional upregulation of the pro-in¯ammatory cytokines TNFa and IL-6. In contrast, there was no change in levels of transcripts for TGFb1, IL-1b, GM-CSF, IL-10, or IL-12. These data provide the ®rst evidence that ovine microglial cells can support productive infection with MVV, and that this leads to a selective upregulation of proin¯ammatory cytokines. These may contribute to visna neuropathology. Journal of NeuroVirology (2000) 6, 320 ± 328.

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Section: Discussionsupporting

confidence: 93%

Phenotypic characterisation and infection of ovine microglial cells with Maedi-Visna Virus

Ebrahimi¹,

Allsopp²,

Fazakerley³

et al. 2000

J Neurovirol

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“…After infection the level of expression of MHC is increased on microglial cells in the central nervous system in sheep (3) and is increased in the infected lung (32) and synovium (1). Infected macrophages therefore have the necessary conditions in tissues and in lesions to present viral antigen to T cells.…”

Section: Discussionmentioning

confidence: 99%

Immune Response to Individual Maedi-Visna VirusgagAntigens

Singh

McConnell

Blacklaws

2006

J Virol

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The lesions caused by maedi-visna virus (MVV) are known to be immune mediated with a presumed contribution by the response to viral antigens. However, very little is known about the T-cell response to individual viral proteins. We have therefore expressed the three individual gag antigens of MVV strain EV1 (p16, p25, and p14) in a bacterial expression system and used the purified recombinant proteins to analyze the antibody and CD4؉ T-cell response to MVV. Plasma samples were taken from sheep after 1 year of infection with MVV. The titers for antibodies in these samples were determined by indirect enzyme-linked immunosorbent assays and were as follows: anti-p25 antibody, 1:400 to >1:3,200; anti-p16 antibody, 1:400 to 1:3,200; and anti-p14 antibody, 1:<100 to 1:3,200. When the induction of antibodies was followed over time postinfection (p.i.), samples positive for anti-p25 were seen by day 24 p.i., followed by anti-p16 by day 45 p.i., and lastly anti-p14 by day 100 p.i. T-cell proliferative responses to all three gag antigens were detected in persistently infected sheep peripheral blood lymphocytes. The antigens were therefore used to raise T-cell lines from persistently infected sheep. These T-cell lines were shown to be specific for the recombinant gag antigens and for viral antigen expressed on infected macrophages. The proliferative response was restricted to major histocompatibility complex class II HLA-DR and so was due to CD4 ؉ T lymphocytes. All three gag antigens may therefore play a role in immune-mediated lesion formation in MVV disease by presentation on infected macrophages in lesions.

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“…There have been several important studies demonstrating involvement of many gene products in SRLV infection and disease [137,138,139,140,141,142,143,144,145,146,147,148,149,150,151,152,153,154,155,156,157,158,159,160,161,162], but these do not specifically relate to individual genetic variants present in sheep. In addition to building understanding of infection and disease, such valuable results prepare the way for further work to address whether such genetic variants exist in small ruminants, and if so, begin developing genetic marker tests.…”

Section: Development Of Genetic Marker Tests For Small Ruminant Lementioning

confidence: 99%

Expanding Possibilities for Intervention against Small Ruminant Lentiviruses through Genetic Marker-Assisted Selective Breeding

White

Knowles

2013

Viruses

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Small ruminant lentiviruses include members that infect sheep (ovine lentivirus [OvLV]; also known as ovine progressive pneumonia virus/maedi-visna virus) and goats (caprine arthritis encephalitis virus [CAEV]). Breed differences in seroprevalence and proviral concentration of OvLV had suggested a strong genetic component in susceptibility to infection by OvLV in sheep. A genetic marker test for susceptibility to OvLV has been developed recently based on the TMEM154 gene with validation data from over 2,800 sheep representing nine cohorts. While no single genotype has been shown to have complete resistance to OvLV, consistent association in thousands of sheep from multiple breeds and management conditions highlight a new strategy for intervention by selective breeding. This genetic marker-assisted selection (MAS) has the potential to be a useful addition to existing viral control measures. Further, the discovery of multiple additional genomic regions associated with susceptibility to or control of OvLV suggests that additional genetic marker tests may be developed to extend the reach of MAS in the future. This review will cover the strengths and limitations of existing data from host genetics as an intervention and outline additional questions for future genetic research in sheep, goats, small ruminant lentiviruses, and their host-pathogen interactions.

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Constitutive and visna virus induced expression of class I and II major histocompatibility complex antigens in the central nervous system of sheep and their role in the pathogenesis of visna lesions

Cited by 11 publications

References 38 publications

Phenotypic characterisation and infection of ovine microglial cells with Maedi-Visna Virus

Phenotypic characterisation and infection of ovine microglial cells with Maedi-Visna Virus

Immune Response to Individual Maedi-Visna VirusgagAntigens

Expanding Possibilities for Intervention against Small Ruminant Lentiviruses through Genetic Marker-Assisted Selective Breeding

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