1998
DOI: 10.1099/0022-1317-79-8-1833
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Viruses and apoptosis.

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Cited by 308 publications
(226 citation statements)
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“…Virus infection has been observed to be associated with apoptosis [8][9][10][11], and the molecular mechanisms and signal pathways have been disclosed in virus infection of mammal cells [12,13]. Apoptosis of fish cells can be also triggered by virus infection [14][15][16], but systematic studies on mitochondrial dynamics and the molecular mechanisms are very limited.…”
Section: Introductionmentioning
confidence: 99%
“…Virus infection has been observed to be associated with apoptosis [8][9][10][11], and the molecular mechanisms and signal pathways have been disclosed in virus infection of mammal cells [12,13]. Apoptosis of fish cells can be also triggered by virus infection [14][15][16], but systematic studies on mitochondrial dynamics and the molecular mechanisms are very limited.…”
Section: Introductionmentioning
confidence: 99%
“…Viruses have evolved novel mechanisms to prevent apoptosis of their host cell and thereby promote virus multiplication (O'Brien, 1998;Roulston et al, 1999). To date, two distinct types of apoptotic suppressor, represented by P35 and the inhibitors of apoptosis (IAPs), have been identi®ed in the invertebrate baculoviruses (Clem, 2001).…”
Section: Introductionmentioning
confidence: 99%
“…Several DNA tumour viruses encode proteins that interact with key regulators of the cell cycle to block apoptosis by inactivation of the tumour suppressor protein p53. Examples include (i) blocking of p53 transcriptional activity following binding of adenovirus E1B 55 kDa protein to p53, (ii) targetting p53 for accelerated degradation by human papillomavirus E6 protein and (iii) blocking of p53 DNA-binding activity mediated by SV40 large T-antigen (Muro-Cacho et al, 1995 ;O'Brien, 1998). Conversely, apoptosis can be blocked independently of tumour suppressor protein inactivation, as exemplified by herpes simplex virus (HSV) type 1-encoded serine\threonine kinase U S 3 (Leopardi et al, 1997) and the lack of programmed cell death as a consequence of Semliki Forest virus (SFV) infection when using p53 -BHK cells (Glasgow et al, 1998).…”
Section: Introductionmentioning
confidence: 99%