Copyright
©2014 Baishideng Publishing Group Inc. All rights reserved.
World J Biol Chem. May 26, 2014; 5(2): 93-105
Published online May 26, 2014. doi: 10.4331/wjbc.v5.i2.93
Published online May 26, 2014. doi: 10.4331/wjbc.v5.i2.93
Regulation of cell survival and death during Flavivirus infections
Sounak Ghosh Roy, Beata Sadigh, Emmanuel Datan, Richard A Lockshin, Zahra Zakeri, Department of Biology, Queens College and Graduate Center of the City University of New York, Queens, New York, NY 11367, United States
Author contributions: Sadigh B and Datan E contributed equally to this paper; all the authors participated in the paper.
Supported by NIAID NIH grant to Zakeri Z, No. 1R15AIO94351-01; the NIH NIGMS (MARC-USTAR), No. T 34 GM070387
Correspondence to: Zahra Zakeri, PhD, Department of Biology, Queens College and Graduate Center of the City University of New York, 65-30 Kissena Blvd, Queens, New York, NY 11367, United States. zahra_zakeri@hotmail.com
Telephone: +1-718-9973417 Fax: + 1-718-9973429
Received: December 17, 2013
Revised: February 27, 2014
Accepted: April 25, 2014
Published online: May 26, 2014
Processing time: 190 Days and 4.4 Hours
Revised: February 27, 2014
Accepted: April 25, 2014
Published online: May 26, 2014
Processing time: 190 Days and 4.4 Hours
Core Tip
Core tip: The pathogenicity of Flaviviruses derives from their ability to infect many types of cells. They can activate both intrinsic and extrinsic pathways of apoptosis, by many means. Dengue and Japanese encephalitis virus can also activate autophagy, whereby autophagy temporarily spares the infected cell, allowing longer reproduction of virus and protecting the cell against other stresses. Given the versatility of these viruses, we need to understand much better how the specific viral proteins affect the pathways to apoptosis and autophagy. Only in this manner will we be able to minimize the pathology that they cause.