Comparative Effects of Bluetongue Virus Infection of Ovine and Bovine Endothelial Cells

Russell, Harold; O’Toole, Donal; Bardsley, Katherine D.; Davis, William C.; Ellis, John

doi:10.1177/030098589603300309

Cited by 23 publications

(18 citation statements)

References 24 publications

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“…Endothelial cells from different tissue origins within the mammalian host also exhibit differences in BTV or AHSV susceptibility and subsequent immune responses [15,41,42]. This suggests that variations in the susceptibility of vascular endothelial cells within different organs of the infected host could potentially determine tissue tropism and “organ-manifestation” of BTV, particularly the localisation of haemorrhages.…”

Section: Discussionmentioning

confidence: 99%

Involvement of the skin during bluetongue virus infection and replication in the ruminant host

Darpel

Monaghan

Simpson

et al. 2012

Veterinary Research

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Bluetongue virus (BTV) is a double stranded (ds) RNA virus (genus Orbivirus; family Reoviridae), which is considered capable of infecting all species of domestic and wild ruminants, although clinical signs are seen mostly in sheep. BTV is arthropod-borne (“arbovirus”) and able to productively infect and replicate in many different cell types of both insects and mammalian hosts. Although the organ and cellular tropism of BTV in ruminants has been the subject of several studies, many aspects of its pathogenesis are still poorly understood, partly because of inherent problems in distinguishing between “virus replication” and “virus presence”.BTV replication and organ tropism were studied in a wide range of infected sheep tissues, by immuno-fluorescence-labeling of non-structural or structural proteins (NS2 or VP7 and core proteins, respectively) using confocal microscopy to distinguish between virus presence and replication. These results are compared to gross and microscopic pathological findings in selected organs from infected sheep. Replication was demonstrated in two major cell types: vascular endothelial cells, and agranular leukocytes which morphologically resemble lymphocytes, monocytes/macrophages and/or dendritic cells. Two organs (the skin and tonsils) were shown to support relatively high levels of BTV replication, although they have not previously been proposed as important replication sites during BTV infection. The high level of BTV replication in the skin is thought to be of major significance for the pathogenesis and transmission of BTV (via biting insects) and a refinement of our current model of BTV pathogenesis is discussed.

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Section: Discussionmentioning

confidence: 99%

Involvement of the skin during bluetongue virus infection and replication in the ruminant host

Darpel

Monaghan

Simpson

et al. 2012

Veterinary Research

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“…This constituted the first evidence of in vitro IFN production in response to BTV infection. In the following years, BTV was reported to induce IFN in many cell types from various tissues and species including foetal and adult leukocytes and spleen cells from sheep (Rinaldo et al, 1975), endothelial cells from bovine and ovine origin (Coen et al, 1991;Russell et al, 1996;Chauveau et al, 2012) and kidney cells from rabbits, hamsters, monkeys, cats and pigs (Jameson and Grossberg, 1981;Fulton and Pearson, 1982;Taylor and O'Brien, 1985). Importantly, BTV was also shown to induce the production of IFN in multiple human cells with a high efficiency particularly in tumour-derived cell lines (Jameson and Grossberg, 1978, 1979, 1981Joklik, 1981;Chauveau et al, 2012).…”

Section: Btv Induces Type I Ifn Production Both In Vitro and In Vivomentioning

confidence: 99%

Induction and control of the type I interferon pathway by Bluetongue virus

et al. 2014

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The innate immune response is the first line of defence against viruses, involving the production of type I IFN (IFN-α/β) and other pro-inflammatory cytokines that control the infection. It also shapes the adaptive immune response generated by both T and B cells. Production of type I IFN occurs both in vivo and in vitro in response to Bluetongue virus (BTV), an arthropod-borne virus. However, the mechanisms responsible for the production of IFN-β in response to BTV remained unknown until recently and are still not completely understood. In this review, we describe the recent advances in the identification of cellular sensors and signalling pathways involved in this process. The RNA helicases retinoic acid-inducible gene-I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5) were shown to be involved in the expression of IFN-β as well as in the control of BTV infection in non-haematopoietic cells. In contrast, induction of IFN-α/β synthesis in sheep primary plasmacytoid dendritic cells (pDCs) required the MyD88 adaptor independently of the Toll-like receptor 7 (TLR7), as well as the kinases dsRNA-activated protein kinase (PKR) and stress-activated protein kinase (SAPK)/Jun N-terminal protein kinase (JNK). As type I IFN is essential for the establishment of an antiviral cellular response, most of viruses have elaborated counteracting mechanisms to hinder its action. This review also addresses the ability of BTV to interfere with IFN-β synthesis and the recent findings describing the non-structural viral protein NS3 as a powerful antagonist of the host cellular response.

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“…BTV is a strong inducer of IFN-I both in vivo and in vitro in multiple cell types derived from various tissues and species (26)(27)(28)(29)(30)(31)(32)(33)(34)(35). Recently, we identified RIG-I and MDA5 helicases as sensors of BTV infection in nonhematopoietic cells and showed that these molecules displayed antiviral activities against the virus (26).…”

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confidence: 99%