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Nitazoxanide, an antiviral thiazolide, depletes ATP-sensitive intracellular Ca2+ stores.
- Source :
-
Virology . Aug2014, Vol. 462, p135-148. 14p. - Publication Year :
- 2014
-
Abstract
- Nitazoxanide (NTZ) inhibits influenza, Japanese encephalitis, hepatitis B and hepatitis C virus replication but effects on the replication of other members of the Flaviviridae family has yet to be defined. The pestivirus bovine viral diarrhoea virus (BVDV) is a surrogate model for HCV infection and NTZ induced PKR and eIF2α phosphorylation in both uninfected and BVDV-infected cells. This led to the observation that NTZ depletes ATP-sensitive intracellular Ca2+ stores. In addition to PKR and eIF2α phosphorylation, consequences of NTZ-mediated Ca2+ mobilisation included induction of chronic sub-lethal ER stress as well as perturbation of viral protein N-linked glycosylation and trafficking. To adapt to NTZ-mediated ER stress, NTZ treated cells upregulated translation of Ca2+-binding proteins, including the ER chaperone Bip and the cytosolic pro-survival and anti-viral protein TCTP. Depletion of intracellular Ca2+ stores is the primary consequence of NTZ treatment and is likely to underpin all antiviral mechanisms attributed to the thiazolide. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 00426822
- Volume :
- 462
- Database :
- Academic Search Index
- Journal :
- Virology
- Publication Type :
- Academic Journal
- Accession number :
- 97389311
- Full Text :
- https://doi.org/10.1016/j.virol.2014.05.015