2006
DOI: 10.1128/jvi.80.8.4114-4121.2006
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Abstract: Neutralization of tumor necrosis factor alpha or Fas ligand had no effect on apoptosis. These results demonstrate that NS1 is sufficient to induce apoptosis in liver-derived cells and that it does so through the initiation of an intrinsic caspase pathway.

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Cited by 64 publications
(75 citation statements)
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“…Interestingly, previous studies have indicated that that B19V can infect immortalized human microvascular endothelial cells and the human hepatocyte cell line HepG2 (18,45), which might play a role in B19V infection-caused myocarditis (4,6) and fulminant hepatitis (5,23,41,48), respectively. EpoR is detectable on endothelial cells (35) and on hepatocytes (44), which may explain the B19V permissiveness of these cells under certain conditions.…”
Section: Discussionmentioning
confidence: 99%
“…Interestingly, previous studies have indicated that that B19V can infect immortalized human microvascular endothelial cells and the human hepatocyte cell line HepG2 (18,45), which might play a role in B19V infection-caused myocarditis (4,6) and fulminant hepatitis (5,23,41,48), respectively. EpoR is detectable on endothelial cells (35) and on hepatocytes (44), which may explain the B19V permissiveness of these cells under certain conditions.…”
Section: Discussionmentioning
confidence: 99%
“…The link between toxicity and apoptosis was first suggested by ultrastructural examination of B19V-infected fetal erythroid progenitors (63,64) and then in an erythroid cell line transfected with the NS1 gene, where activation of caspase 3 was demonstrated (61). The nucleoside triphosphate-binding domain of the NS1 protein of B19V was considered to be involved in B19V-mediated apoptosis in erythroid and nonerythroid cells (61,62,80). Induction of erythroid cell apoptosis by B19V also involves the interaction of NS1 protein with the tumor necrosis factor (TNF) receptor-signaling pathway (87), leading to the activation of caspases 3 and 6.…”
Section: Virus Replication and Cell Apoptosismentioning
confidence: 99%
“…Instead, HBx persistently activated the cyclin B1-CDK1 kinase. The mechanism of G2/M arrest induced by other viral proteins is similar to that of G2/M arrest induced by HBx, such as human parvovirus B19 NS1 protein and human papillomavirus type 16 (HPV16) E1^E4 protein (13,20).…”
Section: Discussionmentioning
confidence: 76%