Wanted: The Paralysis Genes
Can a child’s own genome play a role in acute flaccid myelitis?
When more than 100 children across the U.S. developed a polio-like condition known as acute flaccid myelitis during last fall’s outbreak of enterovirus D-68 (EV-D68), many doctors suspected that the virus caused the disorder.
But the true picture may be much more complicated, says Priya Duggal, PhD ’03, MPH ’98. She points out that even if EV-D68 is the culprit—a contention strengthened by a study recently published in The Lancet—it may have had an accomplice: the sickened children’s own genes.
Duggal, an associate professor of Epidemiology, explains that researchers have yet to establish a definitive causal link between EV-D68 and acute flaccid myelitis, or AFM, which is characterized by muscle weakness and paralysis. Moreover, if EV-D68 or some other virus were solely responsible for AFM, large clusters of victims ought to have appeared. Yet the 115 reported cases were largely sporadic, and likely represented but a small fraction of those who were exposed to the virus. Even siblings who fell ill at the same time didn’t suffer the same neurological effects.
That last fact led Duggal and her colleagues to ask whether the children’s genes might be involved. What if some children were genetically predisposed to develop AFM in response to a particular viral infection while others, including their own siblings, were not?
The researchers now are collecting DNA samples from children who developed AFM during the enterovirus outbreak, and from their unaffected sibs. By sequencing and comparing these whole genomes, the researchers hope to identify the genetic differences that may make some children vulnerable to AFM.