Reactive oxygen species activate NF魏B (p65) and p53 and induce apoptosis in RVFV infected liver cells
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- 作者：Aarthi Narayanan ; Moushimi Amaya ; Kelsey Voss ; Myung Chung ; Ashwini Benedict ; Gavin Sampey ; Kylene Kehn-Hall ; Aless ; ra Luchini ; Lance Liotta ; Charles Bailey ; Ajit Kumar ; Sina Bavari ; Ramin M. Hakami ; Fatah Kashanchi
- 关键词：Reactive oxygen species ; p65 ; p53 ; Apoptosis ; Liver cells ; Rift Valley fever virus
- 刊名：Virology
- 出版年：20 January, 2014
- 年：2014
- 卷：449
- 期：Complete
- 页码：270-286
- 全文大小：6246 K
文摘
Rift Valley fever virus (RVFV) infection is often associated with pronounced liver damage. Previously, our studies revealed altered host phospho-signaling responses (NF魏B, MAPK and DNA damage responses) in RVFV infected epithelial cells that correlated with a cellular stress response. Here, we report that RVFV infection of liver cells leads to an increase in reactive oxygen species (ROS). Our data suggests the presence of the viral protein NSs in the mitochondria of infected cells, hence contributing to early increase in ROS. Increased ROS levels correlated with activation of NF魏B (p65) and p53 responses, which in conjunction with infection, was also reflected as macromolecular rearrangements observed using size fractionation of protein lysates. Additionally, we documented an increase in cytokine expression and pro-apoptotic gene expression with infection, which was reversed with antioxidant treatment. Collectively, we identified ROS and oxidative stress as critical contributors to apoptosis of liver cells during RVFV infection.