Recruitment of TRADD, FADD, and caspase 8 to double-stranded RNA-triggered death inducing signaling complexes (dsRNA-DISCs)

Iordanov, Mihail S.; Kirsch, Julian; Ryabinina, Olga P.; Wong, John; Spitz, Paul; Korcheva, Veselina; Thorburn, Andrew; Magun, Bruce E.

doi:10.1007/s10495-005-6071-x

Cited by 26 publications

(27 citation statements)

References 15 publications

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“…However, the molecular pathway is not as straightforward as appears to be at first glance. Since E3L is known to bind dsRNA we tested induction of BH3-only proteins through dsRNA and found that expression of Noxa was induced (this was very recently also reported by others 27 although another group recently reported findings suggesting that dsRNA induces apoptosis not through Noxa but through the formation of a caspase-8-activating protein complex 38,39 ). Indeed, Noxa expression was induced upon infection with MVA-DE3L.…”

Section: Discussionmentioning

confidence: 52%

Modified vaccinia virus Ankara protein F1L is a novel BH3-domain-binding protein and acts together with the early viral protein E3L to block virus-associated apoptosis

Fischer¹,

Ludwig

Holzapfel³

et al. 2005

Cell Death Differ

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Infection with viruses often protects the infected cell against external stimuli to apoptosis. Here we explore the balance of apoptosis induction and inhibition for infection with the modified vaccinia virus Ankara (MVA), using two MVA mutants with experimentally introduced deletions. Deletion of the E3L-gene from MVA transformed the virus from an inhibitor to an inducer of apoptosis. Noxa-deficient mouse embryonic fibroblasts (MEF) were resistant to MVA-DE3L-induced apoptosis. When the gene encoding F1L was deleted from MVA, apoptosis resulted that required Bak or Bax. MVA-DF1L-induced apoptosis was blocked by Bcl-2. When expressed in HeLa cells, F1L blocked apoptosis induced by forced expression of the BH3-only proteins, Bim, Puma and Noxa. Finally, biosensor analysis confirmed direct binding of F1L to BH3 domains. These data describe a molecular framework of how a cell responds to MVA infection by undergoing apoptosis, and how the virus blocks apoptosis by interfering with critical steps of its signal transduction.

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Section: Discussionmentioning

confidence: 52%

Modified vaccinia virus Ankara protein F1L is a novel BH3-domain-binding protein and acts together with the early viral protein E3L to block virus-associated apoptosis

Fischer¹,

Ludwig

Holzapfel³

et al. 2005

Cell Death Differ

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“…Most often protein kinase R (PKR) activation takes place during viral infection, activating apoptosis via the extrinsic (caspase 8) and the intrinsic (caspase 9) pathway. The activation of caspase 8 is, in this case, independent from death receptors on the cell surface (Balachandran et al, 1998;Gil & Esteban, 2000;Iordanov et al, 2005). Kolokoltsova et al (2014) showed JUNV-induced apoptosis in Huh7 and A549 cells, which was RIG-I-dependent and IFN-Iindependent, an observation that is consistent with the finding that some RNA viruses can trigger mitochondrial apoptosis via a RIG-I/MAVS-dependent pathway involving IRF3 (Chattopadhyay et al, 2010(Chattopadhyay et al, , 2011, and indeed this might also be the case for TCRV.…”

Section: Discussionmentioning

confidence: 98%

The New World arenavirus Tacaribe virus induces caspase-dependent apoptosis in infected cells

Wolff

Groseth

Meyer

et al. 2016

Journal of General Virology

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The Arenaviridae is a diverse and growing family of viruses that already includes more than 25 distinct species. While some of these viruses have a significant impact on public health, others appear to be non-pathogenic. At present little is known about the host cell responses to infection with different arenaviruses, particularly those found in the New World; however, apoptosis is known to play an important role in controlling infection of many viruses. Here we show that infection with Tacaribe virus (TCRV), which is widely considered the prototype for non-pathogenic arenaviruses, leads to stronger induction of apoptosis than does infection with its human-pathogenic relative Junín virus. TCRV-induced apoptosis occurred in several cell types during late stages of infection and was shown to be caspase-dependent, involving the activation of caspases 3, 7, 8 and 9. Further, UV-inactivated TCRV did not induce apoptosis, indicating that the activation of this process is dependent on active viral replication/transcription. Interestingly, when apoptosis was inhibited, growth of TCRV was not enhanced, indicating that apoptosis does not have a direct negative effect on TCRV infection in vitro. Taken together, our data identify and characterize an important virus-host cell interaction of the prototypic, non-pathogenic arenavirus TCRV, which provides important insight into the growing field of arenavirus research aimed at better understanding the diversity in responses to different arenavirus infections and their functional consequences.

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“…dsRNA can probably activate a 'classical' apoptosis pathway similar to that activated by TNF. Consistent with this, dsRNA treatment leads to the formation of a complex containing both FADD and procaspase-8 (Iordanov et al, 2005), with subsequent cleavage of procaspase-8 to the active form (Iordanov et al, 2005;Takahashi et al, 2006). The formation of this complex may involve PKR (Balachandran et al, 1998(Balachandran et al, , 2000a.…”

Section: Induction Of Ifn By Virusesmentioning

confidence: 90%

Interferons and viruses: an interplay between induction, signalling, antiviral responses and virus countermeasures

Randall

Goodbourn

2008

Journal of General Virology

1,369

1,405

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The interferon (IFN) system is an extremely powerful antiviral response that is capable of controlling most, if not all, virus infections in the absence of adaptive immunity. However, viruses can still replicate and cause disease in vivo, because they have some strategy for at least partially circumventing the IFN response. We reviewed this topic in 2000 [Goodbourn, S., Didcock, L. & Randall, R. E. (2000). J Gen Virol 81, 2341-2364] but, since then, a great deal has been discovered about the molecular mechanisms of the IFN response and how different viruses circumvent it. This information is of fundamental interest, but may also have practical application in the design and manufacture of attenuated virus vaccines and the development of novel antiviral drugs. In the first part of this review, we describe how viruses activate the IFN system, how IFNs induce transcription of their target genes and the mechanism of action of IFN-induced proteins with antiviral action. In the second part, we describe how viruses circumvent the IFN response. Here, we reflect upon possible consequences for both the virus and host of the different strategies that viruses have evolved and discuss whether certain viruses have exploited the IFN response to modulate their life cycle (e.g. to establish and maintain persistent/latent infections), whether perturbation of the IFN response by persistent infections can lead to chronic disease, and the importance of the IFN system as a species barrier to virus infections. Lastly, we briefly describe applied aspects that arise from an increase in our knowledge in this area, including vaccine design and manufacture, the development of novel antiviral drugs and the use of IFN-sensitive oncolytic viruses in the treatment of cancer. Biology of the interferon systemThe interferons (IFNs) are a group of secreted cytokines that elicit distinct antiviral effects. They are grouped into three classes called type I, II and III IFNs, according to their amino acid sequence. Type I IFNs (discovered in 1957;Isaacs & Lindenmann, 1957) comprise a large group of molecules; mammals have multiple distinct IFN-a genes (13 in man), one to three IFN-b genes (one in man) and other genes, such as IFN-v, -e, -t, -d and -k. The IFN-a and -b genes are induced directly in response to viral infection, whereas IFN-v, -e, -d and -k play less well-defined roles, such as regulators of maternal recognition in pregnancy. Thus, rather than use the term 'type I IFN', we will use IFN-a/b when referring to the virally induced cytokines. Although the multigenic nature of IFN-a has been known for over 20 years, the significance of this is still debatedi.e. whether these genes are expressed differentially in distinct cell types, whether they are inducible by different types of viruses or whether they are functionally specialized (Brideau-Andersen et al., 2007). For the rest of this review, we will not distinguish between IFN-a subtypes. Type III IFNs have been described more recently and comprise IFNl1, -l2 and -l3, also referred to as IL-2...

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Recruitment of TRADD, FADD, and caspase 8 to double-stranded RNA-triggered death inducing signaling complexes (dsRNA-DISCs)

Cited by 26 publications

References 15 publications

Modified vaccinia virus Ankara protein F1L is a novel BH3-domain-binding protein and acts together with the early viral protein E3L to block virus-associated apoptosis

Modified vaccinia virus Ankara protein F1L is a novel BH3-domain-binding protein and acts together with the early viral protein E3L to block virus-associated apoptosis

The New World arenavirus Tacaribe virus induces caspase-dependent apoptosis in infected cells

Interferons and viruses: an interplay between induction, signalling, antiviral responses and virus countermeasures

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