A false-colored, negative-stained transmission electron micrograph of an influenza virus particle or virion. Orange-colored proteins stud the white lipid membrane. The internal matrix space is colored brown; the capsid is colored purple. Image courtesy of Frederick Murphy, CDC
Battling the bug
The influenza virus presents an on-going, ever-changing challenge to doctors and scientists. By constantly mutating, by promiscuously and randomly swapping genetic material, the “flu bug” is a different beast every year, forcing researchers to develop vaccines in anticipation of strains they think will be most dominant.
Prevention of the flu is a notoriously complicated business; so too is treating it.
In a new paper, published in the journal Cell, Edward A. Dennis, PhD, distinguished professor of pharmacology, chemistry and biochemistry at the University of California, San Diego School of Medicine, Oswald Quechenberger, PhD, professor of medicine and colleagues at Seattle BioMed, St. Jude Children’s Research Hospital, and the University of Washington describe the complex and varied roles of lipid mediators, which contradictorily both drive the miseries of the flu and help resolve them.
Lipid mediators are a class of signaling molecules involved in recruiting immune cells to the site of an infection. In this role, mediators help provoke the inflammatory response that flu sufferers glumly experience as its characteristic aches, pains, swelling, fever and more.
The new research expands and deepens understanding of what lipid mediators do. After infection, some mediators act as anti-inflammatory agents. “Lipid mediators, including ones derived from the omega-3 fatty acids found in fish oil and known as DHA and EPA, are also involved in resolving inflammation and bringing the body back to homeostasis,” observed Quehenberger and Dennis.
These contrary abilities suggest mediators may represent a new target for flu therapies.
“By identifying the pro- and anti-inflammatory mediators as they change over the time course of infection,” said Dennis, “we can identify new enzyme and receptor targets for therapy. Once an infection starts, it’s too late for vaccines. Although anti-viral agents could potentially stop the expansion of the virus, by discovering the mediators, elucidating their pathways and identifying the enzymes/receptors involved, we can develop new targets for drug treatment of active influenza infections.”