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

UMD researcher seeks a unified approach to disarming the large group of pathogens known as enteroviruses.

Cells that have been manipulated to fluoresce green when the phospholipid synthesis process is active reveal an uninfected cell on the left and an infected cell on the right.

Image Credit: George Belov / University of Maryland

April 12, 2022 Kimbra Cutlip

Associate Professor George Belov from the Department of Veterinary Medicine at the University of Maryland received $2M from NIH to study a new method to combat enterovirus infections.

Enteroviruses are 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.

Belov’s research will investigate ways to interrupt 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.


This research is being supported by the National Institute Of Allergy And Infectious Diseases of the National Institutes of Health under Award Number R01AI169458. The content in this story is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.