MicroRNAs regulate immunometabolism—how the immune system alters the metabolic state to combat infection

Posted on Friday, December 11, 2015

OTTAWA, December 11, 2015 -- Many viruses use their host’s metabolism for important building blocks and energy requirements in order to extend their own life cycle. To combat infection, humans have evolved mechanisms to block viruses’ access to these key resources.

A group of scientists, led by Professor John Pezacki from the Department of Chemistry and Biomolecular Sciences and PhD student Ragunath Singaravelu, is exploring the key molecules that control access by viruses to the human body’s main structural and energy components. The team has identified a small molecule in the liver, called microRNA-185, that inhibits the expression of metabolic genes required for the synthesis of fatty acids and cholesterol.

The study suggests that during viral infection in the liver our immune system increases microRNA-185 levels to suppress liver fat biosynthesis and impede viral infection. The researchers have also identified a virus that actively decreases microRNA-185 levels, which then promotes fat accumulation in the liver and circumvents our immune response. Overall, this work highlights microRNA-185 as a novel mediator of the innate immune response through regulation of liver metabolism.

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