Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8751935 | Virus Research | 2018 | 12 Pages |
Abstract
The role of Ca2+ during dengue virus (DENV) replication is unknown; thus, changes in Ca2+ homeostasis in DENV infected human hepatic HepG2 and Huh-7 cells were analyzed. Infected HepG2 cells, but not Huh-7 cells, showed a significant increase in plasma membrane permeability to Ca2+, while both cell lines showed marked reduced levels of Ca2+ stored in the endoplasmic reticulum. While the expression levels of STIM1 and ORAI1 showed no changes, STIM1 and ORAI1 were shown to co-localized in infected cells, indicating activation of the store-operated Ca2+ entry (SOCE) pathway. Finally, manipulation in the infected cells of the intra and extracellular Ca2+ levels by chelators (BAPTA-AM and EGTA), SOC inhibitor (SKF96365), IP3 Receptor antagonist (2APB) or increase of extracellular [Ca2+], significantly reduced DENV yield, but not vesicular stomatitis virus yield, used as a control. These results show that DENV infection alters cell Ca2+ homeostasis and that such changes favor viral replication.
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Authors
Cinthia L. Dionicio, Franshelle Peña, Luis A. Constantino-Jonapa, Carlos Vazquez, Martha Yocupicio-Monroy, Romel Rosales, José Luis Zambrano, Marie Christine Ruiz, Rosa M. del Angel, Juan E. Ludert,