Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/170721
Title: The mechanism of cell death during West Nile virus infection is dependent on initial infectious dose
Authors: Chu, JJH 
Ng, ML 
Keywords: Animals
Apoptosis
Caspase 3
Caspase 9
Caspases
Cell Death
Chlorocebus aethiops
Cytochalasin B
Cytochromes c
Cytokines
HMGB1 Protein
L-Lactate Dehydrogenase
Mitochondria
Poly(ADP-ribose) Polymerases
Time Factors
Vero Cells
West Nile virus
Issue Date: 1-Dec-2003
Publisher: Microbiology Society
Citation: Chu, JJH, Ng, ML (2003-12-01). The mechanism of cell death during West Nile virus infection is dependent on initial infectious dose. Journal of General Virology 84 (12) : 3305-3314. ScholarBank@NUS Repository.
Abstract: 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.
Source Title: Journal of General Virology
URI: https://scholarbank.nus.edu.sg/handle/10635/170721
ISSN: 00221317
14652099
Appears in Collections:Staff Publications
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