1998
DOI: 10.1046/j.1365-2443.1998.00164.x
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Type I interferons are essential mediators of apoptotic death in virally infected cells

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Cited by 141 publications
(103 citation statements)
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References 45 publications
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“…Earlier reports suggested that virus-induced apoptosis was dependent on the action of IFNs (Tanaka et al, 1998). Even though it remains to be determined how different viruses or other factors influence apoptosis, our results demonstrate that although activation of NOXA and induction of apoptosis by SV occur concomitantly with production of type I IFNs, both apoptosis and induction of NOXA are unaffected by the presence of neutralizing anti-IFN a/b antibody, strongly suggesting that SV-induced apoptosis is IFN independent.…”
Section: Discussionsupporting
confidence: 55%
See 1 more Smart Citation
“…Earlier reports suggested that virus-induced apoptosis was dependent on the action of IFNs (Tanaka et al, 1998). Even though it remains to be determined how different viruses or other factors influence apoptosis, our results demonstrate that although activation of NOXA and induction of apoptosis by SV occur concomitantly with production of type I IFNs, both apoptosis and induction of NOXA are unaffected by the presence of neutralizing anti-IFN a/b antibody, strongly suggesting that SV-induced apoptosis is IFN independent.…”
Section: Discussionsupporting
confidence: 55%
“…Although virus-induced cytolysis has all the hallmarks of apoptosis (Tanaka et al, 1998;Licata and Harty, 2003), the mechanisms underlying this effect are poorly understood. The data presented in this report show that virus-induced apoptosis is accompanied by transcriptional upregulation of NOXA and that this event is independent of p53 activation but is dependent on the activation of IRF-1, IRF-3 and CREB.…”
Section: Discussionmentioning
confidence: 99%
“…IFN produced in response to virus infection plays an essential role in inducing apoptosis in virus-infected cells (3,9,52). The infected host organisms are thought to inhibit and eliminate viral infection by sacrificing virus-infected cells through apoptosis.…”
Section: Discussionmentioning
confidence: 99%
“…The exact mechanisms of IFN-promoted apoptosis in virus-infected cells are not clear. It is thought that IFN can activate caspases and up-regulate expression of genes with proapoptotic functions such as death factors (3,9,52). In rSV5V⌬C-infected HeLa cells, increased IFN production was detected and the IFN signaling pathway was intact.…”
Section: Discussionmentioning
confidence: 99%
“…The integration of bidirectional vectors within actively transcribed genes might be problematic considering that the cellular RNA running over the viral LTR boundaries will ultimately result in the formation of dsRNA that can trigger nuclear and cytoplasmic dsRNA responses and subsequent A-I editing of the message, reduced cap-dependent translation or cell death. 24,54,55 Finally, we showed a proof of principle for the use of bidirectional vectors in human CD34+ cells, for the efficient Cre-mediated recombination of indicator cells as well as MGMT-P140K-mediated protection of hematopoietic cells along with efficient cell tracking by fluorescence marker expression. The bidirectional vector system benefits from the generation of two independent messages with coordinated expression.…”
Section: Improving Bidirectional Vector Performancementioning
confidence: 95%