Journal
VIROLOGY
Volume 422, Issue 1, Pages 6-12Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2011.09.023
Keywords
Rift Valley fever virus; RVFV; Interferon; Tumor necrosis factor; Immunity; Cytokine; Monocyte; Macrophage; Survival; Hemorrhagic fever
Categories
Funding
- Intramural CDC HHS [CC999999] Funding Source: Medline
Ask authors/readers for more resources
Rift Valley fever virus (RVFV) causes significant morbidity and mortality in humans and livestock throughout Africa and the Middle East. The clinical disease ranges from mild febrile illness, to hepatitis, retinitis, encephalitis and fatal hemorrhagic fever. RVFV NSs protein has previously been shown to interfere in vitro with the interferon response, and RVFV lacking the NSs protein is attenuated in several animal models. Monocytes and macrophages are key players in the innate immune response via expression of various cytokines and chemokines. Here we demonstrate that wild-type RVFV infection of human monocyte-derived macrophages leads to a productive infection and inhibition of the innate immune response via decreased expression of IFN-alpha 2, IFN-beta and TNF-alpha. Using a recombinant virus lacking the NSs protein, we show that this effect is mediated by the viral NSs protein. Finally, analysis of RVF patient samples demonstrated an association between a pro-inflammatory cytokine response and patient survival. Published by Elsevier Inc.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available