Linked Life Data

14645911

Source:http://linkedlifedata.com/resource/pubmed/id/14645911

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
Pt 12
pubmed:dateCreated
2003-12-3
pubmed:abstractText
The mechanism of West Nile (WN) virus-induced cell death is determined by the initial infectious dose. In Vero cells infected with WN virus at an m.o.i. of 10 or greater, morphological changes characteristic of necrosis were observed as early as 8 h post-infection (p.i.). Pathological changes included extensive cell swelling and loss of plasma membrane integrity, as revealed by optical and electron microscopy. High extracellular lactate dehydrogenase (LDH) activity was observed together with leakage of the high mobility group 1 (HMGB1) protein into the extracellular space. When cells undergo necrosis, they release the HMGB1 protein, a pro-inflammatory mediator cytokine. At high infectious doses, loss of cell plasma membrane integrity was due to the profuse budding of WN progeny virus particles during maturation. When this profuse budding process was disrupted using cytochalasin B, LDH activity was reduced dramatically. In contrast, WN virus-induced cell killing occurred predominantly by apoptosis when cells were infected with an m.o.i. of </=1; the process of apoptosis observed was much later after infection (32 h p.i.). Fragmentation of DNA, chromatin condensation and formation of apoptotic bodies were all observed. This WN virus-induced apoptosis pathway was initiated by the release of cytochrome c from the mitochondria and was accompanied by the formation of apoptosomes. In turn, this led to the activation of caspase-9 and -3, and to the cleavage of the poly(ADP-ribose) polymerase.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0022-1317
pubmed:author
pubmed:issnType
Print
pubmed:volume
84
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3305-14
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
The mechanism of cell death during West Nile virus infection is dependent on initial infectious dose.
pubmed:affiliation
Flavivirology Laboratory, Department of Microbiology, 5 Science Drive 2, National University of Singapore, 117597 Singapore.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't