Phylogenetic analysis of small ruminant lentiviruses detected in Slovenia

Kuhar, Urška; Barlič–Maganja, Darja; Grom, Jože

doi:10.1016/j.vetmic.2012.08.024

Cited by 19 publications

(21 citation statements)

References 16 publications

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“…In addition to the recent classification of SRLV subgroups 1 and 2 that associate with sheep TMEM154 E35K genotypes, SRLVs from around the world have been typed into major genotype groups A-E, and into subtypes within the genotype groups based on gag and/or pol variation [13,21-23]. To characterize the SRLVs infecting the North Dakota sheep, their gag sequences were compared to 1) those of SRLVs from North America and elsewhere in the world, and 2) the top ten closest blast matches to the gag sequence from one of the infected TMEM154 “4,4” ewes in a Neighbor-Net phylogenetic network (Figure 1) and a Neighbor-Joining tree (Figure 2), (see Additional file 1 for sequence information).…”

Section: Introduction Methods and Resultsmentioning

confidence: 99%

“…SRLV genotype A is highly diverse with 15 subtypes currently known [23]. To better understand the context of ovine TMEM154 allele associations with SRLV infection susceptibility, it would be interesting to know if SRLV members of other A subtypes, genotypes B-E, and any circulating recombinant forms vary by an association with TMEM154 alleles, including an ability to infect sheep with TMEM154 “4,4” diplotypes.…”

Section: Discussionmentioning

confidence: 99%

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Genetic subgroup of small ruminant lentiviruses that infects sheep homozygous for TMEM154 frameshift deletion mutation A4Δ53

Clawson

Redden

Schuller

et al. 2015

Vet Res

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Small ruminant lentivirus (SRLV) infections of sheep are influenced by genetics on both the host and pathogen sides. Genetic variation in the ovine transmembrane 154 (TMEM154) gene associates with infection susceptibility, and distinct SRLV genetic subgroups infect sheep in association with their TMEM154 diplotypes. In this study, a novel SRLV subgroup was identified that naturally infected sheep with various TMEM154 diplotypes, including those homozygous for a rare frameshift mutation (A4 delta53), which is predicted to abolish TMEM154 protein function. Thus, these SRLVs may infect sheep that lack functional TMEM154, and may not be restricted by TMEM154 diplotypes in establishing infections.Electronic supplementary materialThe online version of this article (doi:10.1186/s13567-015-0162-7) contains supplementary material, which is available to authorized users.

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Section: Introduction Methods and Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Genetic subgroup of small ruminant lentiviruses that infects sheep homozygous for TMEM154 frameshift deletion mutation A4Δ53

Clawson

Redden

Schuller

et al. 2015

Vet Res

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“…SRLV complete genomes have been sequenced and are available in the GenBank derived from goat (CAEV-CO [59,60], 1GA [61,62], Gansu [63], Shanxi [64], FESC-752 [25], Seui [46] Roccaverano [45] and A4 [27] viruses) and sheep (Fonni [30], Volterra [30], 496 [65], SA-OMVV [66], KV1514 [67], KV1772 [68], LV1 [69], EV1 [70], P1OLV [71], 85/34 [72] and 697 [73] viruses) (Figure 1). In addition, partial sequences have been published in Brazil [74,75,76], Canada [77], Finland [78], France [27,79,80,81], Greece [82], Ireland [83], Japan [84], Netherlands [85], Poland [86,87], Russia [88], Slovenia [89], South Korea [90] and Turkey [29,30]. …”

Section: Phylogenymentioning

confidence: 99%

Small Ruminant Lentiviruses: Genetic Variability, Tropism and Diagnosis

Ramírez

Reina

Amorena

et al. 2013

Viruses

100

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Small ruminant lentiviruses (SRLV) cause a multisystemic chronic disease affecting animal production and welfare. SRLV infections are spread across the world with the exception of Iceland. Success in controlling SRLV spread depends largely on the use of appropriate diagnostic tools, but the existence of a high genetic/antigenic variability among these viruses, the fluctuant levels of antibody against them and the low viral loads found in infected individuals hamper the diagnostic efficacy. SRLV have a marked in vivo tropism towards the monocyte/macrophage lineage and attempts have been made to identify the genome regions involved in tropism, with two main candidates, the LTR and env gene, since LTR contains primer binding sites for viral replication and the env-encoded protein (SU ENV), which mediates the binding of the virus to the host’s cell and has hypervariable regions to escape the humoral immune response. Once inside the host cell, innate immunity may interfere with SRLV replication, but the virus develops counteraction mechanisms to escape, multiply and survive, creating a quasi-species and undergoing compartmentalization events. So far, the mechanisms of organ tropism involved in the development of different disease forms (neurological, arthritic, pulmonary and mammary) are unknown, but different alternatives are proposed. This is an overview of the current state of knowledge on SRLV genetic variability and its implications in tropism as well as in the development of alternative diagnostic assays.

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“…Small Ruminant Lentivirus (SRLV) infection is spreading all over the world, with new descriptions in countries such as Poland [1], Sultanate of Oman, Canada [2], Slovenia [3], Russia [4] and new genotypes such as A12, A14 and A15 [3], E and B3 [5-7]. Today, highly efficient prophylactic/therapeutic measures against SRLV do not exist, and control is frequently based on early diagnosis and culling of seropositive ewes and their progeny.…”

Section: Introductionmentioning

confidence: 99%

Small ruminant macrophage polarization may play a pivotal role on lentiviral infection

Crespo

Bertolotti

Juganaru

et al. 2013

Vet Res

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Small ruminant lentiviruses (SRLV) infect the monocyte/macrophage lineage inducing a long-lasting infection affecting body condition, production and welfare of sheep and goats all over the world. Macrophages play a pivotal role on the host’s innate and adaptative immune responses against parasites by becoming differentially activated. Macrophage heterogeneity can tentatively be classified into classically differentiated macrophages (M1) through stimulation with IFN-γ displaying an inflammatory profile, or can be alternatively differentiated by stimulation with IL-4/IL-13 into M2 macrophages with homeostatic functions. Since infection by SRLV can modulate macrophage functions we explored here whether ovine and caprine macrophages can be segregated into M1 and M2 populations and whether this differential polarization represents differential susceptibility to SRLV infection. We found that like in human and mouse systems, ovine and caprine macrophages can be differentiated with particular stimuli into M1/M2 subpopulations displaying specific markers. In addition, small ruminant macrophages are plastic since M1 differentiated macrophages can express M2 markers when the stimulus changes from IFN-γ to IL-4. SRLV replication was restricted in M1 macrophages and increased in M2 differentiated macrophages respectively according to viral production. Identification of the infection pathways in macrophage populations may provide new targets for eliciting appropriate immune responses against SRLV infection.

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Phylogenetic analysis of small ruminant lentiviruses detected in Slovenia

Cited by 19 publications

References 16 publications

Genetic subgroup of small ruminant lentiviruses that infects sheep homozygous for TMEM154 frameshift deletion mutation A4Δ53

Genetic subgroup of small ruminant lentiviruses that infects sheep homozygous for TMEM154 frameshift deletion mutation A4Δ53

Small Ruminant Lentiviruses: Genetic Variability, Tropism and Diagnosis

Small ruminant macrophage polarization may play a pivotal role on lentiviral infection

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