Avian reovirus-triggered apoptosis enhances both virus spread and the processing of the viral nonstructural muNS protein

Rodríguez-Grille, Javier; Busch, Lisa K.; Martı́nez-Costas, José; Benavente, Javier

doi:10.1016/j.virol.2014.04.039

Cited by 18 publications

(12 citation statements)

References 43 publications

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“…Recently, two independent studies on ARV-induced apoptosis have concluded that ARV-induced apoptosis is favorable for virus spread and increasing the viral yield [19,31]. Our data seem contrary to those presented in those two papers, but in fact, their results and ours may actually be compatible.…”

Section: Discussioncontrasting

confidence: 99%

Critical role of eukaryotic elongation factor 1 alpha 1 (EEF1A1) in avian reovirus sigma-C-induced apoptosis and inhibition of viral growth

Zhang

Lin

et al. 2015

Arch Virol

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Avian reovirus (ARV) causes viral arthritis, chronic respiratory diseases, retarded growth and malabsorption syndrome. It is well established that the ARV sigma-C protein induces apoptosis in host cells. However, the underlying molecular mechanism of this induction is still unclear. We report here the identification of eukaryotic elongation factor 1 alpha 1 (EEF1A1) as the interacting partner of σC. We found that σC-induced apoptosis in DF-1 cells could be completely abolished by knockdown of EEF1A1 by siRNA. Furthermore, knockdown of EEF1A1 markedly reduced ARV-induced apoptosis associated with decreased caspase-9 and -3 activation and cytochrome C release, leading to increased ARV growth in host cells. Thus, EEF1A1 plays a critical role in σC-induced apoptosis and inhibition of viral growth.

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Section: Discussioncontrasting

confidence: 99%

Critical role of eukaryotic elongation factor 1 alpha 1 (EEF1A1) in avian reovirus sigma-C-induced apoptosis and inhibition of viral growth

Zhang

Lin

et al. 2015

Arch Virol

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“…In spite of the presence of TLR4 ligand (LPS), EcN colonization resulted in a more substantial decrease of apoptotic and TLR4 expressing MNCs than LGG, emphasizing the complexity of the TLR signaling pathways. Virus‐triggered apoptosis is a conserved innate immune defense strategy of eliminating virus infected cells; however, it may also aid the pathogen by facilitating its spread . Therefore, the EcN and LGG‐mediated counteraction of the HRV‐induced apoptosis that we observed in this study could have limited the HRV replication.…”

Section: Discussionmentioning

confidence: 75%

Escherichia coli Nissle 1917 protects gnotobiotic pigs against human rotavirus by modulating pDC and NK‐cell responses

et al. 2016

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Gram-positive lactic acid-producing bacteria including Lactobacillus rhamnosus GG (LGG) are commonly used as probiotics, while fewer gram-negative probiotics including Escherichia coli Nissle 1917 (EcN) are characterized. A mechanistic understanding of their individual and interactive effects on human rotavirus (HRV) disease and immunity is lacking. Noncolonized, EcN, LGG and EcN+LGG-colonized neonatal gnotobiotic (Gn) pigs were challenged with HRV. EcN colonization associated with greater protection against HRV, also induced the highest frequencies of plasmacytoid dendritic cells (DC), significantly increased natural killer (NK) cell function and decreased frequencies of apoptotic and TLR4+ mononuclear cells (MNCs). Consistent with the highest NK cell activity, splenic CD172+ MNCs (DC enriched fraction) of EcN colonized pigs produced the highest levels of IL-12 (activates NK cells) in vitro. LGG colonization had little effect on the above parameters, and those of EcN+LGG colonized pigs were intermediate, suggesting that the probiotics modulate each other’s effects. Additionally, in vitro EcN-treated splenic or intestinal MNCs produced a higher but balanced cytokine repertoire (IFN-α, IL-12 and IL-10), as compared to that of pigs treated with LGG. These results indicate that the EcN-mediated greater protection against HRV was associated with potent stimulation of the innate immune system and activation of the DC-IL-12-NK immune axis.

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“…The M 115 residue was determined to be the best candidate as M 94 is not conserved among all PRV isolates, and M 85 and M 169 are unlikely due to the sizes of the proteins generated. Post-translational cleavage to generate µNSC as shown for ARV µNS cannot be excluded, although the specific proteolytic cleavage site in the ARV protein is not conserved in PRV [2,33,53]. The different µNS size variants, i.e., full-length µNS and the 70 kDa variant with putative translation initiation at M 115 , may differ in their interactions with other PRV proteins.…”

Section: Discussionmentioning

confidence: 99%

Viral Protein Kinetics of Piscine Orthoreovirus Infection in Atlantic Salmon Blood Cells

Haatveit

Wessel

Markussen

et al. 2017

Viruses

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Piscine orthoreovirus (PRV) is ubiquitous in farmed Atlantic salmon (Salmo salar) and the cause of heart and skeletal muscle inflammation. Erythrocytes are important target cells for PRV. We have investigated the kinetics of PRV infection in salmon blood cells. The findings indicate that PRV causes an acute infection of blood cells lasting 1–2 weeks, before it subsides into persistence. A high production of viral proteins occurred initially in the acute phase which significantly correlated with antiviral gene transcription. Globular viral factories organized by the non-structural protein µNS were also observed initially, but were not evident at later stages. Interactions between µNS and the PRV structural proteins λ1, µ1, σ1 and σ3 were demonstrated. Different size variants of µNS and the outer capsid protein µ1 appeared at specific time points during infection. Maximal viral protein load was observed five weeks post cohabitant challenge and was undetectable from seven weeks post challenge. In contrast, viral RNA at a high level could be detected throughout the eight-week trial. A proteolytic cleavage fragment of the µ1 protein was the only viral protein detectable after seven weeks post challenge, indicating that this µ1 fragment may be involved in the mechanisms of persistent infection.

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Avian reovirus-triggered apoptosis enhances both virus spread and the processing of the viral nonstructural muNS protein

Cited by 18 publications

References 43 publications

Critical role of eukaryotic elongation factor 1 alpha 1 (EEF1A1) in avian reovirus sigma-C-induced apoptosis and inhibition of viral growth

Critical role of eukaryotic elongation factor 1 alpha 1 (EEF1A1) in avian reovirus sigma-C-induced apoptosis and inhibition of viral growth

Escherichia coli Nissle 1917 protects gnotobiotic pigs against human rotavirus by modulating pDC and NK‐cell responses

Viral Protein Kinetics of Piscine Orthoreovirus Infection in Atlantic Salmon Blood Cells

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