A “decoy” molecule that can curb a runaway inflammatory response to the flu virus has been uncovered in a new study.

The body’s immune response is built from an inflammatory attack intended to kill the virus. If the attack gets too aggressive, tghough, this counterattack can end up damaging the body’s own tissues, resulting in damage that can lead to death.

Now, in addition to finding the decoy molecule, a University of Maryland researcher has uncovered new details about how this response works.

The researcher, Vladimir Y. Toshchakov, Ph.D., assistant professor in the University of Maryland School of Medicine, said:

“We think this molecule has real potential as a strategy to protect patients from the body’s tendency to respond too strongly to some viruses."

Toshchakov investigated a molecule called 2R9, which can block signals from the toll-like receptors.

2R9 is known as a “decoy” molecule because it finds its way into the sequence of signals, and so blocks the signals, stopping the communication that leads to the inflammation.

In experiments on mice that were particularly vulnerable to flu, he found that 2R9 had a strong effect.

In mouse the group treated with the molecule, only 22 percent died. In comparison, the group that did not receive 2R9, had around a 90 percent mortality rate.

Even without a massive outbreak, like the 1918 Swine Flu epidemic that killed 18 million people, flu is still a serious public health threat. The illness annually kills between 22,000 and 28,000 Americans, according to the Centers for Disease Control and Prevention.

Toshchakov added that 2R9 did not totally stop immune response to the flu virus. This is important because a homeostatic balance is necessary.

If the body mounts no attack on the virus, the virus will thrive and spread, causing harm and perhaps death.

But too much response is also harmful. 2R9 seems to modulate the response safely in the middle of these extremes.

Toshchakov also looked at how 2R9 interacted with human cells.

It appears to have a similar affect as in mice. This indicates that using it makes sense to continue testing the molecule as a potential human treatment.

“Eventually, we want to see whether this compound, and this pathway, can help treat people with the flu,” says Toshchakov.

Journal reference: Cell Reports DOI: http://dx.doi.org/10.1016/j.celrep.2015.05.035

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