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$2M NIH Grant Will Help Develop a New Defense Against Viral ‘Hijackers’

Researcher Seeks Unified Approach to Disarming Large Group of Pathogens Known as Enteroviruses

By Kimbra Cutlip


Enteroviruses cause a host of illnesses with no effective way to fight them. Now, a UMD researcher is working to stop a key ability of enteroviruses to "hijack" a cell's ability to build its own internal parts to facilitate the infection.

Illustration by iStock

A University of Maryland researcher has received $2 million from the National Institutes of Health to study a new method to combat a large, diverse group of viruses that can cause everything from stomach flu and rashes to polio and hand foot and mouth disease.

There are no effective medical treatments for enteroviruses, in large part because they are very good at developing resistance to therapeutics, but Associate Professor George Belov in the Department of Veterinary Medicine is working to counter this ability.

Belov’s research will investigate interruption of a critical step that occurs in all enterovirus infections: the development of something called replication organelles. Enteroviruses hijack the system a cell uses to build its internal parts, commanding that system to build membranes to support the virus’s own replication machinery. The membrane creates a new organelle inside an infected cell that hides the virus’s replication machinery from the cell’s immune defenses.

In previous studies, Belov showed that, once a cell is infected with an enterovirus, its machinery for producing the building blocks of organelle membranes rapidly kicks into gear. This new grant will enable him to develop methods to manipulate or interrupt that machinery, preventing the production of those building blocks, known as phospholipids. By short circuiting the development of replication organelles in this way, Belov’s new methods will open new directions for controlling the infections that rely on them.

“Perhaps you can target those specific pathways that the virus induced in the cell to build new structures,” he said. “You could make the virus more visible to the cell so that it can more rapidly communicate the infected state to the immune system, or you can inhibit the development of those new structures and directly prevent viral replication.”

All enteroviruses appear to trigger the production of phospholipids, so targeting the cell’s own mechanism for creating phospholipids rather than some unique feature of a given virus could avoid the problem of viruses evolving defenses against therapeutic drugs. And, targeting that cellular process could lead to broad-spectrum therapies against all enterovirus infections.



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