Abstract
Primate blood cells were analysed for changes in global gene expression patterns at several time points following infection with Ebola virus, providing insights into potential mechanisms of viral pathogenesis and host defense.
Highlights
Infection with Ebola virus (EBOV) causes a fulminant and often fatal hemorrhagic fever
Sudan Ebola virus and Zaire Ebola virus (ZEBOV) have been associated with human disease outbreaks in Central Africa, with case fatality rates averaging about 50% for Sudan Ebola virus and ranging from 75% to 90% for ZEBOV [2]
We previously identified a set of genes representing the TNFα/nuclear factor-κB (NF-κB) B regulon as a prominent feature of the peripheral blood mononuclear cell (PBMC) response to bacterial lipopolysaccharide [22]
Summary
Infection with Ebola virus (EBOV) causes a fulminant and often fatal hemorrhagic fever. Ebola virus causes severe and often lethal hemorrhagic fever in humans and nonhuman primates. The EBOV genus consists of four distinct species: Ivory Coast Ebola virus, Reston Ebola virus, Sudan Ebola virus, and Zaire Ebola virus (ZEBOV) [1]. Sudan Ebola virus and ZEBOV have been associated with human disease outbreaks in Central Africa, with case fatality rates averaging about 50% for Sudan Ebola virus and ranging from 75% to 90% for ZEBOV [2]. Reston Ebola virus is highly lethal in nonhuman primates [3,4], the few data available suggest that it is nonpathogenic in humans [5]. There are no approved preventive vaccines or postexposure treatments for EBOV hemorrhagic fever, but recent advances have led to the development of several candidate therapeutics and vaccines for EBOV [9,10,11]
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