Full Text:   <2177>

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CLC number: R183.7

On-line Access: 2015-01-05

Received: 2014-12-15

Revision Accepted: 2014-12-23

Crosschecked: 2014-12-16

Cited: 8

Clicked: 5165

Citations:  Bibtex RefMan EndNote GB/T7714




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Journal of Zhejiang University SCIENCE B 2015 Vol.16 No.1 P.1-9


Against Ebola: type I interferon guard risk and mesenchymal stromal cell combat sepsis

Author(s):  Lei Zhang, Hao Wang, Yi-qing Zhang

Affiliation(s):  Tianjin International Joint Academy of Biomedicine, Tianjin 300457, China; more

Corresponding email(s):   biotech@china.com

Key Words:  Ebola, Type I interferon, Mesenchymal stromal cell, Non-specific immune modulation

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Lei Zhang, Hao Wang, Yi-qing Zhang. Against Ebola: type I interferon guard risk and mesenchymal stromal cell combat sepsis[J]. Journal of Zhejiang University Science B, 2015, 16(1): 1-9.

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The 2014 ebola outbreak in West Africa trig-gered a global crisis. Nine countries have reported more than 20000 infection cases in total and nearly 8000 lives have been lost. The actual death toll is likely much higher than this figure; the death rate is as high as 70%, considering confirmed cases. The ebola virus launches its destruction by shutting down the host’s innate and adaptive immune systems. The virus then replicates itself out of control and causes a cytokine storm in the host. Consequently, the host’s overdriven immune system attacks its own endothelial cells and this leads to multiple organ hemorrhagic damage, the host dies of septic shock finally. Under current circumstances where no specific interventions have shown effectiveness against the virus, our opinions are justified in applying a non-specific anti-viral approach during the incubation period of virus infection as an essential protection to put the host’s immune system into an alert state and henceforth to slow down the viral replication. When the viral infection proceeds to the terminal stage, the key factor would be applying a non-specific immune modulation approach to suppress the cytokine storm that causes multiple organ failure, in an attempt to open a time window for the host’s immune system to recover.




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