SrasV1, PubMed, Curation, bibRecord, 001024

Multi-organ lesions in suckling mice infected with SARS-associated mammalian reovirus linked with apoptosis induced by viral proteins μ1 and σ1.

Identifieur interne : 001024 ( PubMed/Curation ); précédent : 001023; suivant : 001025

Multi-organ lesions in suckling mice infected with SARS-associated mammalian reovirus linked with apoptosis induced by viral proteins μ1 and σ1.

Auteurs : Lihua Song [République populaire de Chine] ; Yongfeng Lu [République populaire de Chine] ; Jun He [République populaire de Chine] ; Yonghui Yu [République populaire de Chine] ; Tingting Zuo [République populaire de Chine] ; Yanwei Li [République populaire de Chine] ; Hong Zhu [République populaire de Chine] ; Qing Duan [République populaire de Chine]

Source :

PloS one [ 1932-6203 ] ; 2014.

RBID : pubmed:24664247

Descripteurs français

KwdFr :
- Animaux, Animaux allaités, Apoptose, Cellules HEK293, Humains, Infections à Reoviridae (anatomopathologie), Infections à Reoviridae (génétique), Protéines de capside (génétique), Protéines de capside (métabolisme), Reoviridae (métabolisme), Reoviridae (physiologie), Souris, Virus du SRAS (physiologie).
MESH :
- anatomopathologie : Infections à Reoviridae.
- génétique : Infections à Reoviridae, Protéines de capside.
- métabolisme : Protéines de capside, Reoviridae.
- physiologie : Reoviridae, Virus du SRAS.
- Animaux, Animaux allaités, Apoptose, Cellules HEK293, Humains, Souris.

English descriptors

KwdEn :
- Animals, Animals, Suckling, Apoptosis, Capsid Proteins (genetics), Capsid Proteins (metabolism), HEK293 Cells, Humans, Mice, Reoviridae (metabolism), Reoviridae (physiology), Reoviridae Infections (genetics), Reoviridae Infections (pathology), SARS Virus (physiology).
MESH :
- chemical , genetics : Capsid Proteins.
- chemical , metabolism : Capsid Proteins.
- genetics : Reoviridae Infections.
- metabolism : Reoviridae.
- pathology : Reoviridae Infections.
- physiology : Reoviridae, SARS Virus.
- Animals, Animals, Suckling, Apoptosis, HEK293 Cells, Humans, Mice.

Abstract

We reported the isolation and characterization of a novel mammalian reassortant reovirus BYD1 that may have played an accomplice role with SARS-coronavirus during the 2003 SARS pandemic. The pathogenic mechanism of this novel reovirus is unknown. Reovirus pathogenicity has been associated with virus-induced apoptosis in cultured cells and in vivo. The reovirus outer capsid protein μ1 is recognized as the primary determinant of reovirus-induced apoptosis. Here, we investigated the apoptosis induced by BYD1, its outer capsid protein μ1, and its cell-attachment protein σ1 to understand the pathogenesis of BYD1. We also investigated BYD1 caused systemic complications in suckling mice. Under electron microscopy, BYD1-infected cells showed characteristics typical of apoptosis. Notably, ectopically expressed μ1 and σ1 induced similar pathological apoptosis, independent of BYD1 infection, in host cells in which they were expressed, which suggests that μ1 and σ1 are both apoptotic virulence factors. Consistent with previous reports of reovirus pathogenicity, suckling mice intracranially inoculated with BYD1 developed central nerve damage, myocarditis, and pneumonia. Collectively, our data suggest that BYD1 μ1- and σ1-induced apoptosis is involved in the multi-organ lesions in a suckling mouse BYD1 infection model.

DOI: 10.1371/journal.pone.0092678
PubMed: 24664247

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Le document en format XML

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<front><div type="abstract" xml:lang="en">We reported the isolation and characterization of a novel mammalian reassortant reovirus BYD1 that may have played an accomplice role with SARS-coronavirus during the 2003 SARS pandemic. The pathogenic mechanism of this novel reovirus is unknown. Reovirus pathogenicity has been associated with virus-induced apoptosis in cultured cells and in vivo. The reovirus outer capsid protein μ1 is recognized as the primary determinant of reovirus-induced apoptosis. Here, we investigated the apoptosis induced by BYD1, its outer capsid protein μ1, and its cell-attachment protein σ1 to understand the pathogenesis of BYD1. We also investigated BYD1 caused systemic complications in suckling mice. Under electron microscopy, BYD1-infected cells showed characteristics typical of apoptosis. Notably, ectopically expressed μ1 and σ1 induced similar pathological apoptosis, independent of BYD1 infection, in host cells in which they were expressed, which suggests that μ1 and σ1 are both apoptotic virulence factors. Consistent with previous reports of reovirus pathogenicity, suckling mice intracranially inoculated with BYD1 developed central nerve damage, myocarditis, and pneumonia. Collectively, our data suggest that BYD1 μ1- and σ1-induced apoptosis is involved in the multi-organ lesions in a suckling mouse BYD1 infection model. </div>
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<Abstract><AbstractText>We reported the isolation and characterization of a novel mammalian reassortant reovirus BYD1 that may have played an accomplice role with SARS-coronavirus during the 2003 SARS pandemic. The pathogenic mechanism of this novel reovirus is unknown. Reovirus pathogenicity has been associated with virus-induced apoptosis in cultured cells and in vivo. The reovirus outer capsid protein μ1 is recognized as the primary determinant of reovirus-induced apoptosis. Here, we investigated the apoptosis induced by BYD1, its outer capsid protein μ1, and its cell-attachment protein σ1 to understand the pathogenesis of BYD1. We also investigated BYD1 caused systemic complications in suckling mice. Under electron microscopy, BYD1-infected cells showed characteristics typical of apoptosis. Notably, ectopically expressed μ1 and σ1 induced similar pathological apoptosis, independent of BYD1 infection, in host cells in which they were expressed, which suggests that μ1 and σ1 are both apoptotic virulence factors. Consistent with previous reports of reovirus pathogenicity, suckling mice intracranially inoculated with BYD1 developed central nerve damage, myocarditis, and pneumonia. Collectively, our data suggest that BYD1 μ1- and σ1-induced apoptosis is involved in the multi-organ lesions in a suckling mouse BYD1 infection model. </AbstractText>
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Multi-organ lesions in suckling mice infected with SARS-associated mammalian reovirus linked with apoptosis induced by viral proteins μ1 and σ1.

Multi-organ lesions in suckling mice infected with SARS-associated mammalian reovirus linked with apoptosis induced by viral proteins μ1 and σ1.

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