Differences in the capacity of reovirus strains to induce apoptosis are determined by the viral attachment protein sigma 1

Tyler, Kenneth L.; Squier, Margaret; Rodgers, Steven E.; Schneider, Benjamin E.; Oberhaus, Stephanie M.; Grdina, Theresa A.; Cohen, John; Dermody, Terence S.

doi:10.1128/jvi.69.11.6972-6979.1995

Cited by 188 publications

(153 citation statements)

References 74 publications

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“…In cultured cells, MRV-induced apoptosis is not dependent on de novo synthesis of viral RNA and protein (Connolly and Dermody, 2002;Danthi et al, 2006), indicating that components of the incoming viral capsid are sufficient for initiation of prodeath signaling. Consistent with these findings, differences in the capacity of prototype reovirus strains to induce apoptosis segregate genetically with the S1 and M2 gene segments (Tyler et al, 1995(Tyler et al, , 1996Connolly et al, 2001), which encode the viral attachment protein σ1 and the viral membrane penetration protein μ1, respectively (McCrae and Joklik, 1978;Mustoe et al, 1978). Although initial studies suggested that attachment of MRV σ1 with JAM-A or sialic acid on the host cells is important for apoptosis Connolly et al, 2001), antibody-dependent uptake of MRV virions into host cells in a JAM-A-and sialic acid-independent manner also leads to apoptotic cell death, indicating that signaling pathways triggered by σ1-receptor interactions are dispensable for MRV-induced apoptosis (Danthi et al, 2006).…”

Section: Apoptosis Induction By Delivery Of Viral Components Into Thesupporting

confidence: 57%

Enter the kill zone: Initiation of death signaling during virus entry

Danthi

2011

Virology

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Infection of host cells by a variety of viruses results in programmed cell death or apoptosis. In many cases, early events in virus replication that occur prior to synthesis of viral proteins and replication of viral genomes directly or indirectly activate signaling pathways that culminate in cell death. Using examples of viruses for which prodeath signaling is better defined, this review will describe how cell entry steps including virus attachment to receptors, virus uncoating in endosomes, and events that occur following membrane penetration lead to apoptosis. The relevance and physiologic consequences of early induction of prodeath signaling to viral pathogenesis also will be discussed.

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Section: Apoptosis Induction By Delivery Of Viral Components Into Thesupporting

confidence: 57%

Enter the kill zone: Initiation of death signaling during virus entry

Danthi

2011

Virology

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“…Inhibitors were added immediately following adsorption. The percentage of dead cells after 48 h of incubation was determined by using acridine orange-ethidium bromide (AOEB) staining as described previously (82). For identifying host regulators of cell death, cells were transfected with siRNA as described above and incubated for 48 h prior to infection with T3D.…”

Section: Cells and Virusesmentioning

confidence: 99%

Viral RNA at Two Stages of Reovirus Infection Is Required for the Induction of Necroptosis

Berger

Hiller

Thete

et al. 2017

J Virol

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Necroptosis, a regulated form of necrotic cell death, requires the activation of the RIP3 kinase. Here, we identify that infection of host cells with reovirus can result in necroptosis. We find that necroptosis requires sensing of the genomic RNA within incoming virus particles via cytoplasmic RNA sensors to produce type I interferon (IFN). While these events that occur prior to the synthesis of viral RNA are required for the induction of necroptosis, they are not sufficient. The induction of necroptosis also requires late stages of reovirus infection. Specifically, efficient synthesis of double-stranded RNA (dsRNA) within infected cells is required for necroptosis. These data indicate that viral RNA interfaces with host components at two different stages of infection to induce necroptosis. This work provides new molecular details about events in the viral replication cycle that contribute to the induction of necroptosis following infection with an RNA virus. An appreciation of how cell death pathways are regulated following viral infection may reveal strategies to limit tissue destruction and prevent the onset of disease. Cell death following virus infection can occur by apoptosis or a regulated form of necrosis known as necroptosis. Apoptotic cells are typically disposed of without activating the immune system. In contrast, necroptotic cells alert the immune system, resulting in inflammation and tissue damage. While apoptosis following virus infection has been extensively investigated, how necroptosis is unleashed following virus infection is understood for only a small group of viruses. Here, using mammalian reovirus, we highlight the molecular mechanism by which infection with a dsRNA virus results in necroptosis.

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“…DNAcontaining viruses that induce apoptosis include adenoviruses (Rao et al, 1992;Chiou et al, 1994;Antoni et al, 1995), Epstein±Barr virus (Gregory et al, 1994), and poxviruses (Ray et al, 1992;Hu et al, 1994). Several RNAcontaining viruses have also been reported to induce apoptosis: these include polioviruses (Tolskaya et al, 1995b), Sindbis virus (Levine et al, 1993;Esolen et al, 1995), reovirus (Tyler et al, 1995), and influenza viruses (Takizawa et al, 1993;Fesq et al, 1994). Apoptosis is characterized by distinctive morphological and biochemical features.…”

Section: Introductionmentioning

confidence: 99%

Coronavirus MHV-3-Induced Apoptosis in Macrophages

et al. 1998

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Infection with mouse hepatitis virus strain 3 (MHV-3) results in lethal fulminant hepatic necrosis in fully susceptible BALB/c mice compared to the minimal disease observed in resistant strain A/J mice. Macrophages play a central role in the pathogenesis of MHV-3-induced hepatitis. In the present study we have shown that MHV-3 infection of macrophages induces these cells to undergo apoptosis. Three methods to detect apoptosis were applied: flow cytometry analysis of nuclear DNA content, fluorescence microscopic visualization of apoptotic cells labeled by the TUNEL assay, and gel electrophoresis to detect DNA laddering. Apoptosis in A/J and BALB/c macrophages was first detected at 8 h postinfection (p.i.) and reached a maximum by 12 h p.i. The degree of MHV-3-induced apoptosis was much greater in A/J-derived macrophages than in BALB/c-derived cells. Apoptosis was inversely correlated with the development of typical MHV cytopathology, namely syncytia formation. Infected macrophages from A/J mice did not form synctia in contrast to the extensive synctia formation observed in BALB/c-derived macrophages. In MHV-3-infected BALB/c macrophage cultures, apoptotic cells were not incorporated into syncytia. Apoptosis was also inversely correlated with the expression of MHV-3-induced fgl2 prothrombinase in macrophages. These results add the murine coronavirus MHV-3 to the list of RNA-containing viruses capable of inducing apoptosis.

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Differences in the capacity of reovirus strains to induce apoptosis are determined by the viral attachment protein sigma 1

Cited by 188 publications

References 74 publications

Enter the kill zone: Initiation of death signaling during virus entry

Enter the kill zone: Initiation of death signaling during virus entry

Viral RNA at Two Stages of Reovirus Infection Is Required for the Induction of Necroptosis

Coronavirus MHV-3-Induced Apoptosis in Macrophages

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