From last summer to this March, 115 children in 34 states suddenly developed sudden unexplained paralysis—called acute flaccid myelitis (AFM)—that has kept medical experts scratching their heads about what could be causing it. But in new research published on Monday from the University of California, San Francisco (UCSF), researchers suggest a specific strain of a common virus could be contributing.
Scientists and doctors have long thought that an enterovirus called EV-D68 somehow played a role in the clusters of kids who became partially paralyzed, since the emergence of their symptoms happened at the same time U.S. emergency rooms experienced an unprecedented wave of children coming in with severe EV-D68. But in children who’ve been tested for the virus, it’s very rarely been found in their spinal fluid—the location doctors expect to find it if it’s responsible for paralysis.
The other problem is that enteroviruses are incredibly common, so discovering the virus in children is by no means an anomaly. That makes it difficult to pin the paralysis problem on EV-D68. But now, UCSF scientists have discovered more evidence to link the two. In their study, published in the journal The Lancet Infectious Diseases, the researchers analyze 25 cases of sudden unexplained paralysis from recent clusters of children. Through nasal swabs, the researchers were able to identify EV-D68 in 12 of those children and found that all of the cases testing positive for the virus were related to a strain called B1, which emerged four years ago with mutations similar to those seen in the polio virus. Even though some of the children in the study were from Colorado and others were from California, they shared the same B1 strain of the virus.
The researchers also discovered this specific strain in the blood of one of the children who developed AFM for the first time. The child was sampled much earlier than the others, though, and researchers think the late timing of testing may have been the reason they didn’t detect the virus in the blood or spinal fluid of most of the children. Even though the researchers couldn’t identify EV-D68 in the children’s spinal fluid, they say they’re not ruling it out, since they also couldn’t find any other infections.
Notably, the researchers also studied the virus in a pair of siblings. One sibling developed AFM, but the other remained normal after symptoms of the respiratory disease went away. This suggests that the reactions to the virus could be genetic, the researchers say.
“The question is, is this coincidental or [are the two] really associated? I think it’s more than a coincidence,” says study author Dr. Charles Chiu, director of UCSF-Abbott Viral Diagnostics and Discovery Center. “I think our study answers some of those questions.”
The researchers also sequenced the genome of EV-D68 in six children with AFM and two children without it. They hope that analyzing the virus can help inform future research.
“What’s needed at this point is fundamental biology,” says Chiu. He and his team plan to infect the cells of sibling pairs, where one child got AFM and the other did not, to see if their cells respond differently. Any differences the researchers discover may lead to more knowledge about the underlying causes of the disorder, they say.