Retroviral Infections in Sheep and Goats: Small Ruminant Lentiviruses and Host Interaction

Larruskain, Amaia; Jugo, Begoña M.

doi:10.3390/v5082043

Cited by 60 publications

(50 citation statements)

References 127 publications

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“…Approaching potential genetic factors for MV susceptibility from a different point of view, existing data in diverse species indicated that CCR5 could be a candidate gene for resistance to various pathogens [ 16 , 22 – 27 ]. Even more important in the context of this study is that humans carrying CCR5 variants seem not to acquire human immunodeficiency virus (HIV) [ 28 – 30 ], the best-explored lentivirus.…”

Section: Introductionmentioning

confidence: 99%

First survey on association of TMEM154 and CCR5 variants with serological maedi-visna status of sheep in German flocks

Molaee

Eltanany

Lühken

2018

Vet Res

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Maedi-visna, a disease caused by small ruminant lentiviruses (SRLVs), is present in sheep from many countries, also including Germany. An amino acid substitution (E/K) at position 35 of the transmembrane protein 154 (TMEM154) as well as a deletion in the chemokine (C-C motif) receptor type 5 gene (CCR5) were reported to be associated with the serological MV status and/or the SRLV provirus concentration in North American sheep populations. The aim of this study was to test if those two gene variants might be useful markers for MV susceptibility in Germany. For this purpose, more than 500 sheep from 17 serologically MV positive German sheep flocks with different breed backgrounds were genotyped applying PCR-based methods. Both, crosstab and non-parametric analyses showed significant associations of the amino acid substitution at position 35 of TMEM154 with the serological MV status (cut-off-based classification) and the median MV ELISA S/P value in all samples and in two of the four analyzed breed subsets. The deletion in the CCR5 promoter did not show a consistent association with serological MV status or median ELISA S/P value. It can be concluded that the amino acid substitution at position 35 of TMEM154 is a promising marker for breeding towards a lower number of serologically MV positive sheep in German flocks, at least in flocks of the Texel breed, while this remains questionable for the deletion in the CCR5 promoter. The findings of this study still need to be verified in additional sheep breeds.Electronic supplementary materialThe online version of this article (10.1186/s13567-018-0533-y) contains supplementary material, which is available to authorized users.

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Section: Introductionmentioning

confidence: 99%

First survey on association of TMEM154 and CCR5 variants with serological maedi-visna status of sheep in German flocks

Molaee

Eltanany

Lühken

2018

Vet Res

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“…Although there is indication for association between TMEM154 mutations and control of MVV infection, there is no proven association for all the haplotypes [73]. Other genes associated with virus susceptibility are the DPPA2 (Developmental Pluripotency Associated 2)/DPPA4 (Developmental Pluripotency Associated 4), SYTL3 (Synaptotagmin-Like 3), CCR5 (Chemokine receptor 5), MHC (Major Histocompatability Complex), TLR7, TLR8, TLR9 (Toll-like receptors) genes, and APOBEC3 (Apolipoprotein B mRNA-editing enzyme) proteins [75][76][77], whereas the zinc finger cluster, C19orf42 (Chromosome 19 Open Reading Frame 19)/TMEM38A (Transmembrane Protein 38A) and DLGAP1 (Discs Large (Drosophila) Homolog-Associated Protein 1) genes may be used in genetic selection programs to facilitate the control of the disease [78]. The tripartite motif-containing 5 (TRIM5) protein has been studied and has been proved to contribute to the restriction of MVV [79].…”

Section: Risk Factorsmentioning

confidence: 99%

Etiology, Epizootiology and Control of Maedi-Visna in Dairy Sheep: A Review

Kalogianni

Bossis

Ekateriniadou³

et al. 2020

Animals

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Maedi-visna (MV) in sheep is caused by maedi-visna virus (MVV), a small ruminant lentivirus (SRLV) that causes chronic infection and inflammatory lesions in infected animals. Pneumonia and mastitis are its predominant clinical manifestations, and the tissues infected by MVV are mainly the lungs, the mammary gland, the nervous system and the joints. MV has a worldwide distribution with distinct MVV transmission patterns depending on circulating strains and regionally applied control/eradication schemes. Nevertheless, the prevalence rate of MV universally increases. Currently, gaps in understanding the epizootiology of MV, the continuous mutation of existing and the emergence of new small ruminant lentiviruses (SRLVs) strains, lack of an effective detection protocol and the inefficiency of currently applied preventive measures render elimination of MV an unrealistic target. Therefore, modifications on the existing MV surveillance and control schemes on an evidentiary basis are necessary. Updated control schemes require the development of diagnostic protocols for the early and definitive diagnosis of MVV infections. The objectives of this review are to summarize the current knowledge in the epizootiology and control of MV in dairy sheep, to describe the research framework and to cover existing gaps in understanding future challenges regarding MV.

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“…[7][8][9]12 Future discoveries and advances in understanding the biology of SRLV-host interactions are essential in identifying means to control viral transmission, the resultant disease manifestation, or both.…”

Section: Host Geneticsmentioning

confidence: 99%

Small Ruminant Lentiviruses: Strain Variation, Viral Tropism, and Host Genetics Influence Pathogenesis

Highland

2017

Vet Pathol

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Retroviral Infections in Sheep and Goats: Small Ruminant Lentiviruses and Host Interaction

Cited by 60 publications

References 127 publications

First survey on association of TMEM154 and CCR5 variants with serological maedi-visna status of sheep in German flocks

First survey on association of TMEM154 and CCR5 variants with serological maedi-visna status of sheep in German flocks

Etiology, Epizootiology and Control of Maedi-Visna in Dairy Sheep: A Review

Small Ruminant Lentiviruses: Strain Variation, Viral Tropism, and Host Genetics Influence Pathogenesis

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