Infection kinetics, prostacyclin release and cytokine-mediated modulation of the mechanism of cell death during bluetongue virus infection of cultured ovine and bovine pulmonary artery and lung microvascular endothelial cells

DeMaula, Christopher D.; Jutila, Mark A.; Wilson, Dennis W; Maclachlan, Nigel J

doi:10.1099/0022-1317-82-4-787

Cited by 72 publications

(105 citation statements)

References 41 publications

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“…2H and I, the amounts of IFN-␤ BTV induces the expression of antiviral and proinflammatory genes. Some studies suggest that a major link exists between BTV-induced inflammatory cytokines and the pathogenesis of the disease (8,9). Thus, we decided to investigate the expression of a proinflammatory cytokine whose induction is dependent predominantly on nuclear factor B (NF-B) (i.e., interleukin-8 [IL-8]) and antiviral genes that are regulated mostly by IRF3 (i.e., that for RANTES) or the IFN-␣/␤ response pathway and are so-called IFN-stimulated genes (ISGs; i.e., those for ISG56 and PKR).…”

Section: Resultsmentioning

confidence: 99%

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Sensing and Control of Bluetongue Virus Infection in Epithelial Cells via RIG-I and MDA5 Helicases

Chauveau

Doceul

Lara

et al. 2012

J Virol

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Bluetongue virus (BTV), an arthropod-borne member of the Reoviridae family, is a double-stranded RNA virus that causes an economically important livestock disease that has spread across Europe in recent decades. Production of type I interferon (alpha/beta interferon [IFN-␣/␤]) has been reported in vivo and in vitro upon BTV infection. However, the cellular sensors and signaling pathways involved in this process remain unknown. Here we studied the mechanisms responsible for the production of IFN-␤ in response to BTV serotype 8. Upon BTV infection of A549 cells, expression of IFN-␤ and other proinflammatory cytokines was strongly induced at both the protein and mRNA levels. This response appeared to be dependent on virus replication, since exposure to UV-inactivated virus failed to induce IFN-␤. We also demonstrated that BTV infection activated the transcription factors IFN regulatory factor 3 and nuclear factor B. We investigated the role of several pattern recognition receptors in this response and showed that expression of IFN-␤ was greatly reduced after small-interfering-RNA-mediated knockdown of the RNA helicase encoded by retinoic acid-inducible gene I (RIG-I) or melanoma differentiation-associated gene 5 (MDA5). In contrast, silencing of MyD88, Toll-like receptor 3, or the recently described DexD/H-box helicase DDX1 sensor had no or a weak effect on IFN-␤ induction, suggesting that the RIG-I-like receptor pathway is specifically engaged for BTV sensing. Moreover, we also showed that overexpression of either RIG-I or MDA5 impaired BTV expression in infected A549 cells. Overall, this indicates that RIG-I and MDA5 can both contribute to the recognition and control of BTV infection.

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Section: Resultsmentioning

confidence: 99%

“…Cultures of ECs were purified by fluorescence-activated cell sorting (FACS) on FL2/FL3, with a BD Aria II FACS apparatus as already described (8). The phenotype of the purified ECs was confirmed for PECAM-1 expression (monoclonal antibody [MAb] CD31, catalog no.…”

Section: Cellsmentioning

confidence: 99%

Sensing and Control of Bluetongue Virus Infection in Epithelial Cells via RIG-I and MDA5 Helicases

Chauveau

Doceul

Lara

et al. 2012

J Virol

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“…In mammalian cells, BTV induces cell death (apoptosis and/or necrosis) in cell lines [73], microvascular ovine and bovine endothelial cells [18], monocytes [5] and in WC1-activated T cells [96]. In mammalian cell lines, uncoating of BTV, but not BTV replication, is required to trigger apoptosis [73].…”

Section: Cell Deathmentioning

confidence: 99%

Bluetongue virus: virology, pathogenesis and immunity

et al. 2008

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-Bluetongue (BT) virus, an orbivirus of the Reoviridae family encompassing 24 known serotypes, is transmitted to ruminants via certain species of biting midges (Culicoides spp.) and causes thrombo-hemorrhagic fevers mainly in sheep. During the 20th century, BTV was endemic in sub-tropical regions but in the last ten years, new strains of BTV (serotypes 1, 2, 4, 8, 9, 16) have appeared in Europe leading to a devastating disease in naive sheep and bovine herds (serotype 8). BTV enters into insect cells via the viral inner core VP7 protein and in mammalian cells via the external capsid VP2 haemagglutinin, which is the major determinant of BTV serotype and neutralization. BTV replicates in mononuclear phagocytes and endothelial cells where it induces expression of inflammatory cytokines as well as apoptosis. BTV can remain as nonreplicating entities concealed in erythrocytes for up to five months. Homologous protection against one BTV serotype involves neutralizing antibodies and T cell responses directed to the external VP2 and VP5 proteins, whereas heterologous protection is supported by T cells directed to the NS1 non structural protein and inner core proteins.

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“…9,24,26,47 The association of affected cells with particular anatomic sites has also been described in EHDV and BTV infections. 15,46 Tropism for intravascular monocytes has been described for BTV and EHDV 5,9 and has been observed in infections with EEV (A. D. Pardini, unpublished data, 2007).…”

Section: 5152mentioning

confidence: 99%

Tissue and Cell Tropism of African Horse Sickness Virus Demonstrated by Immunoperoxidase Labeling in Natural and Experimental Infection in Horses in South Africa

Clift

Penrith

2010

Vet Pathol

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Tissues from 196 experimental and confirmed natural cases of African horse sickness (all 9 serotypes) were examined with a standardized and validated immunohistochemical assay for detection of the causative virus. The study confirmed that heart and lung are the main target tissues for African horse sickness virus (across all serotypes), followed closely by spleen. It also indicated that microvascular endothelial cells and monocyte-macrophages are the main target cells for virus replication. The importance of monocytes as target cells was emphasized, with relatively few tissue macrophages containing antigen in the lung and spleen, respectively. The results were largely in agreement with those of previous studies, but the large number of cases examined permitted more precise description of the location and distribution of antigen in different tissues. Comparison with descriptions of tissue and cell tropism of other orbiviruses indicated similarity with African horse sickness. Immunohistochemistry was shown to be a useful and consistent technique for demonstrating target cells, but the difficulty of identifying cell types-in particular, different types of monocyte-macrophages-is a limitation.

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Infection kinetics, prostacyclin release and cytokine-mediated modulation of the mechanism of cell death during bluetongue virus infection of cultured ovine and bovine pulmonary artery and lung microvascular endothelial cells

Cited by 72 publications

References 41 publications

Sensing and Control of Bluetongue Virus Infection in Epithelial Cells via RIG-I and MDA5 Helicases

Sensing and Control of Bluetongue Virus Infection in Epithelial Cells via RIG-I and MDA5 Helicases

Bluetongue virus: virology, pathogenesis and immunity

Tissue and Cell Tropism of African Horse Sickness Virus Demonstrated by Immunoperoxidase Labeling in Natural and Experimental Infection in Horses in South Africa

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