The ZIKA Virus Delays Cell Death Through the Anti-Apoptotic Bcl-2 Family Proteins.
Jonathan TurpinEtienne FrumencePhilippe DesprèsWildriss ViranaïckenPascale Krejbich-TrototPublished in: Cells (2019)
Zika virus (ZIKV) is an emerging human mosquito-transmitted pathogen of global concern, known to be associated with complications such as congenital defects and neurological disorders in adults. ZIKV infection is associated with induction of cell death. However, previous studies suggest that the virally induced apoptosis occurs at a slower rate compared to the course of viral production. In this present study, we investigated the capacity of ZIKV to delay host cell apoptosis. We provide evidence that ZIKV has the ability to interfere with apoptosis whether it is intrinsically or extrinsically induced. In cells expressing viral replicon-type constructions, we show that this control is achieved through replication. Finally, our work highlights an important role for anti-apoptotic Bcl-2 family protein in the ability of ZIKV to control apoptotic pathways, avoiding premature cell death and thereby promoting virus replication in the host-cell.
Keyphrases
- zika virus
- cell death
- cell cycle arrest
- induced apoptosis
- dengue virus
- endoplasmic reticulum stress
- aedes aegypti
- oxidative stress
- signaling pathway
- sars cov
- endothelial cells
- single cell
- high glucose
- cell proliferation
- diabetic rats
- cell therapy
- risk factors
- mesenchymal stem cells
- induced pluripotent stem cells
- mass spectrometry
- case control
- cerebral ischemia