Researchers identify potential drug cure to West Nile-induced memory loss

Though the discovery comes with some worrisome caveats, researchers have begun the journey to reversing the memory loss effects of West Nile virus through the use of a drug.

In a study focused on mice, scientists identified the potential cause of the neurological issues: unresolved inflammation that actively fights the brain’s ability to repair its damaged neurons. By applying an arthritis drug that counteracts the inflammation, researchers found mice gained restored capabilities for learning and memory.

“These memory disturbances make it hard for people to hold down a job, to drive, to take care of all the duties of everyday life,” senior author Robyn Klein, a professor of medicine at Washington University School of Medicine in St. Louis, said. “We found that targeting the inflammation with the arthritis drug could prevent some of these problems with memory.”

More than 10,000 people in the United States currently suffer from memory loss and other neurological issues as a result of West Nile infection. The virus has proven particularly problematic because, during the onset of brain infection, the immune system destroys parts of neurons to fight it off. The result is memory loss, even as the encephalitis leads to permanent fatigue, weakness and other, often worsening traits.

“We started wondering why the damage isn’t repaired after the virus is cleared from the brain,” Klein said. “We know that neurons are produced in the part of the brain involved in learning and memory, so why weren’t new neurons being made after West Nile infection?”

As it turns out, the answer lies in a protein known as IL-1. Mice ill with West Nile were found to produce less neurons and more astrocyte neural cells–normally a nutrition provider for neurons but, under the infection, behaving instead like immune cells, churning out inflammatory proteins. IL-1 is a natural, healthy part of the immune system. It swarms invading viruses and then drops when it’s no longer needed. In West Nile survivors, though, those proteins continue production–and keep new neurons from being produced. Thus, the damage cannot be repaired.

Anakinra, an FDA-approved arthritis drug, interfered with IL-1 when applied and brought inflammation down. Healing began. Mice began to learn again. But it is not a long term solution as it is currently a proof concept. Suppressing IL-1 while the virus is still in the brain could lead to exacerbated encephalitis–and death.

The findings of Klein’s team were published in Nature Immunology.