alteration in superoxide dismutase 1 causes oxidative stress and p38 mapk activation following rvfv infection超氧化物歧化酶1变更导致氧化应激和p38 mapk激活后rvfv感染.pdfVIP
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alteration in superoxide dismutase 1 causes oxidative stress and p38 mapk activation following rvfv infection超氧化物歧化酶1变更导致氧化应激和p38 mapk激活后rvfv感染
Alteration in Superoxide Dismutase 1 Causes Oxidative
Stress and p38 MAPK Activation Following RVFV
Infection
1 1 2 3 1 1
Aarthi Narayanan , Taissia Popova , Michael Turell , Jessica Kidd , Jessica Chertow , Serguei G. Popov ,
1 1 1
Charles Bailey , Fatah Kashanchi *, Kylene Kehn-Hall
1 National Center for Biodefense and Infectious Diseases, George Mason University, Manassas, Virginia, United States of America, 2 Virology Division, United States Army
Medical Research Institute of Infectious Diseases, Fort Detrick, Maryland, United States of America, 3 The Neurological Institute, MDA/ALS Research Center, New York, New
York, United States of America
Abstract
Rift Valley fever (RVF) is a zoonotic disease caused by Rift Valley fever virus (RVFV). RVFV is a category A pathogen that
belongs to the genus Phlebovirus, family Bunyaviridae. Understanding early host events to an infectious exposure to RVFV
will be of significant use in the development of effective therapeutics that not only control pathogen multiplication, but
also contribute to cell survival. In this study, we have carried out infections of human cells with a vaccine strain (MP12) and
virulent strain (ZH501) of RVFV and determined host responses to viral infection. We demonstrate that the cellular
antioxidant enzyme superoxide dismutase 1 (SOD1) displays altered abundances at early time points following exposure to
the virus. We show that the enzyme is down regulated in cases of both a virulent (ZH501) and a vaccine strain (MP12)
exposure. Our data demonstrates that the down regulation of SOD1 is likely to be due to post transcriptional processes and
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