Bluetongue Virus Entry into Cells

Forzan, Mario; Marsh, Mark; Roy, Polly

doi:10.1128/jvi.02284-06

Cited by 86 publications

(103 citation statements)

References 46 publications

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“…BTV core particles can also bind to cells (particularly insect cells) via VP7 trimers. The BTV particle is then internalized in endosomes via a clathrin-dependent endocytosis pathway [26]. VP2 dissociates from the outer capsid layer in early endosomes.…”

Section: Btv Life Cyclementioning

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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Section: Btv Life Cyclementioning

confidence: 99%

Bluetongue virus: virology, pathogenesis and immunity

et al. 2008

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“…4) and is termed the "subcore" (5). The outer capsid is composed of VP2 and VP5, which are necessary for virus entry in mammalian cells (2,5,6). In infected cells BTV encodes four additional nonstructural proteins (NS1, NS2, NS3, and NS3A), which are involved in virus replication and morphogenesis (7)(8)(9)(10).…”

mentioning

confidence: 99%

In vitro reconstitution of Bluetongue virus infectious cores

Lourenco

Roy

2011

Proc. Natl. Acad. Sci. U.S.A.

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Bluetongue virus (BTV) is a vector-borne, nonenveloped icosahedral particle that is organized in two capsids, an outer capsid of two proteins, VP2 and VP5, and an inner capsid (or core) composed of two major proteins, VP7 and VP3, in two layers. The VP3 layer (subcore) encloses viral transcription complex (VP1 polymerase, VP4 capping enzyme, VP6 helicase) and a 10-segmented double-stranded (dsRNA) genome. Although much is known about the BTV capsids, the order of the core assembly and the mechanism of genome packaging remain unclear. Here, we established a cell-free system to reconstitute subcore and core structures with the proteins and ssRNAs, demonstrating that reconstituted cores are infectious in insect cells. Furthermore, we showed that the BTV ssRNAs are essential to drive the assembly reaction and that there is a distinct order of internal protein recruitment during the assembly process. The in vitro engineering of infectious BTV cores is unique for any member of the Reoviridae and will facilitate future studies of RNA-protein interactions during BTV core assembly.assembly pathway | Orbivirus | engineered particle

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“…Following virus attachment and receptor-mediated endocytosis, the virions are uncoated to form core particles. This process is dependent on an acidic pH (Forzan et al, 2007), and is characterized by removal of VP2 and exposure of VP5, which is subsequently responsible for permeabilization of the endosomal membrane to allow the delivery of the transcriptionally active core across the membrane into the cell cytoplasm (Hassan et al, 2001;Zhang et al, 2010). Parental viral particles could therefore trigger apoptosis during receptor engagement, during cell entry or upon virus uncoating.…”

Section: Discussionmentioning

confidence: 99%

“…Following receptor-mediated endocytosis, conversion of the orbivirus virions to core particles that lack the VP2 and VP5 proteins occurs in early endosomes and requires acidic pH (Forzan et al, 2007;Zhang et al, 2010).…”

Section: Induction Of Apoptosis By Ahsv4 In Bhk-21 Cells Requires Virmentioning

confidence: 99%

Virus uncoating is required for apoptosis induction in cultured mammalian cells infected with African horse sickness virus

Vermaak

Theron

2015

Journal of General Virology

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Infection of cultured mammalian cells with African horse sickness virus (AHSV) is known to induce cell death. To date, the trigger(s) of this response, the apoptotic pathways activated during AHSV infection and the functional consequences of apoptosis on the virus replication cycle have yet to be characterized. This study demonstrated that extracellular treatment of BHK-21 cells with both of the AHSV4 outer capsid proteins, VP2 and VP5, was sufficient to trigger apoptosis. Whether steps in AHSV4 replication subsequent to viral attachment were required for AHSV4-induced apoptosis was also investigated. Apoptosis was induced in BHK-21 cells infected with UV-inactivated AHSV4 and in ribavirin-treated cells infected with AHSV4. However, both AHSV4-and VP2/VP5-stimulated apoptotic responses were inhibited in the presence of the endosomal acidification inhibitors ammonium chloride and chloroquine. These results indicated that uncoating of AHSV4 virions, but not viral transcription or subsequent steps in viral replication, was required for AHSV4 to induce apoptosis in BHK-21 cells. Furthermore, this study showed that both the extrinsic (caspase-8) and intrinsic (caspase-9) apoptotic pathways were induced following AHSV4 infection. The inhibition of caspase activity in AHSV4-infected cells did not diminish AHSV4 replication, but reduced the release and dissemination of progeny viral particles. Taken together, the data indicated that uncoating of AHSV virions was required for apoptosis induction, and that apoptosis enhanced virus spread and release.

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Bluetongue Virus Entry into Cells

Cited by 86 publications

References 46 publications

Bluetongue virus: virology, pathogenesis and immunity

Bluetongue virus: virology, pathogenesis and immunity

In vitro reconstitution of Bluetongue virus infectious cores

Virus uncoating is required for apoptosis induction in cultured mammalian cells infected with African horse sickness virus

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