Bluetongue Virus Outer Capsid Proteins Are Sufficient To Trigger Apoptosis in Mammalian Cells

Mórtola, Eduardo; Noad, Rob; Roy, Polly

doi:10.1128/jvi.00802-07

Cited by 17 publications

(42 citation statements)

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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%

Section: Cell Deathmentioning

confidence: 99%

“…In mammalian cell lines, uncoating of BTV, but not BTV replication, is required to trigger apoptosis [73]. Extracellular treatment with a combination of the viral outer capsid proteins VP2 and VP5, and the cell penetration protein VP5 is sufficient to trigger apoptosis, involving activation of NF-B [73]. However, some cell types that support the replication of the virus do not demonstrate a cytopathic effect to BTV, such as insect cells [73], T cell lines [96] and activated blood lymphocytes [5].…”

Section: Cell Deathmentioning

confidence: 99%

“…Extracellular treatment with a combination of the viral outer capsid proteins VP2 and VP5, and the cell penetration protein VP5 is sufficient to trigger apoptosis, involving activation of NF-B [73]. However, some cell types that support the replication of the virus do not demonstrate a cytopathic effect to BTV, such as insect cells [73], T cell lines [96] and activated blood lymphocytes [5]. The budding versus the viroporin-mediated viral exit mechanism might partially explain this difference [104].…”

Section: Cell Deathmentioning

confidence: 99%

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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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Section: Cell Deathmentioning

confidence: 99%

Section: Cell Deathmentioning

confidence: 99%

Section: Cell Deathmentioning

confidence: 99%

Section: Cell Deathmentioning

confidence: 99%

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Bluetongue virus: virology, pathogenesis and immunity

et al. 2008

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“…In the absence of early ie-1 expression in the midgut of AcMNPV-inoculated A. gemmatalis (Fig. 4b), late vp39 expression may have triggered the observed apoptosis in the midgut (Figs 3 and 4b), as has been shown for capsid protein in other viruses including reovirus, West Nile virus, coxsackievirus B3, parvovirus B19 and bluetongue virus (Henke et al, 2000;Mortola et al, 2004;Poole et al, 2004;Clarke et al, 2005;Yang et al, 2008).…”

Section: Midgut Viral Gene Expressionmentioning

confidence: 99%

Pathogenesis of Autographa californica multiple nucleopolyhedrovirus in fifth-instar Anticarsia gemmatalis larvae

Chikhalya¹,

Luu²,

Carrera³

et al. 2009

Journal of General Virology

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We have investigated infection and pathogenesis of Autographa californica multiple nucleopolyhedrovirus (AcMNPV) in Anticarsia gemmatalis (velvetbean caterpillar) larvae using a lacZ recombinant virus (AcMNPV-hsp70/lacZ) to track the temporal progression of infection in the midgut intestine and haemocoel. A. gemmatalis was highly resistant to fatal infection by occlusion bodies (OBs; LD 50 .5.5¾105 OB) and budded virus (BV; LD 50 .3¾10 5 BV) administered via oral and systemic routes, respectively. Orally administered occlusion-derived virus (ODV) efficiently attached and fused to midgut cells; however, high levels of infectioninduced apoptosis limited infection in the midgut. Transcriptional analysis of AcMNPV genes expressed in the midgut of OB-inoculated A. gemmatalis larvae showed high levels of mRNA encoding the major capsid protein VP39 in the absence of immediate-early transactivator 1 (ie-1) expression. In the midgut, virus was efficiently transferred from infected midgut epithelial cells to nearby tracheolar cells and circulating haemocytes to initiate systemic infection in the haemocoel. However, haemocoelic BV did not efficiently disseminate infection and only cuticular epidermal cells displayed high levels of viral infection. Flow cytometry analysis of haemocytes isolated from BV-inoculated A. gemmatalis larvae showed low-level expression of the BV envelope protein GP64 on the cell surface, suggesting that A. gemmatalis haemocytes have a limited capacity for amplifying virus. These results show that AcMNPV is not an effective biological control agent for limiting crop damage caused by A. gemmatalis larvae.

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African horse sickness virus induces apoptosis in cultured mammalian cells

2012

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Infection of mammalian cell cultures with African horse sickness virus (AHSV) is known to result in dramatic cytopathic effects (CPE), but no CPE is observed in infected insect cell cultures despite productive virus replication. The basis for this phenomenon has not yet been investigated, but is suggestive of apoptosis being induced following virus infection of the mammalian cells. To investigate whether AHSV can induce apoptosis in infected mammalian cells, Culicoides variipennis (KC) insect cells and BHK-21 mammalian cells were infected with AHSV-9 and analyzed for morphological and biochemical hallmarks of apoptosis. In contrast to KC cells, infection of BHK-21 cells with AHSV-9 resulted in ultrastructural changes and nuclear DNA fragmentation, both of which are associated with the induction of apoptosis. Results also indicated that AHSV-9 infection of BHK-21 cells resulted in activation of caspase-3, a key agent in apoptosis, and in mitochondrial membrane depolarization. Cumulatively, the data indicate that the intrinsic pathway is activated in AHSVinduced apoptosis.Keywords: African horse sickness virus; Apoptosis; BHK-21 cells; Culicoides variipennis cells; Caspases; Intrinsic pathwayAfrican horse sickness virus (AHSV) is a species in the genus Orbivirus, family Reoviridae (Calisher and Mertens, 1998), and is the causative agent of African horse sickness (AHS), a highly infectious arthropod-borne (Culicoides spp.) disease of equids, of which the mortality rate in horses may exceed 90% (Coetzer and Erasmus, 1994;Guthrie, 2007). Although African horse sickness virus (AHSV) causes severe oedema and haemorrhages in horses, it is asymptomatic in the insect host (Mellor and Hamblin, 2004;Wilson et al., 2009). This is also reflected in tissue culture where AHSV causes rapid cell death in infected mammalian cells in culture, whereas infection of insect cells are unapparent and show no CPE (Mirchamsy et al., 1970;Osawa and Hazrati, 1965). The basis for this differential host response is not known, but may be due to the induction of apoptosis in infected mammalian cells. Indeed, analyses of endothelial cells of animals infected with AHSV indicated ultrastructural changes that could be suggestive of apoptosis (Gómez-Villamandos et al., 1999).Apoptosis is a selective process of physiological cell deletion in response to numerous developmental and environmental stimuli (Kerr et al., 1972). There are two common pathways for the induction of apoptosis, i.e. the extrinsic pathway, which is primarily initiated by virus attachment to receptors, and the intrinsic pathway, which is mediated by damage to the mitochondria (Duprez et al., 2009). Various reports have indicated that infection of mammalian cells by viruses induces apoptosis (Roulston et al., 1999) and in some virus-induced diseases, apoptosis is a pathogenic mechanism that contributes in vivo to cell death, tissue injury and disease severity Samuel et al., 2007). Indeed, the induction of apoptosis has recently been implicated in the pathogenesis of bluetong...

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Bluetongue Virus Outer Capsid Proteins Are Sufficient To Trigger Apoptosis in Mammalian Cells

Cited by 17 publications

References 0 publications

Bluetongue virus: virology, pathogenesis and immunity

Bluetongue virus: virology, pathogenesis and immunity

Pathogenesis of Autographa californica multiple nucleopolyhedrovirus in fifth-instar Anticarsia gemmatalis larvae

African horse sickness virus induces apoptosis in cultured mammalian cells

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