Using a type of chip tiled with thousands of protein fragments from viruses, his group found enterovirus antibodies in 11 of 14 A.F.M. patients, compared to only three of 16 patients with other neurological diseases. And a protein sequence specific to EV-D68 was found in spinal fluid of six A.F.M. patients and blood of eight A.F.M. patients.
“Both studies do provide very compelling evidence that enteroviruses are involved,” Dr. Lynfield said.
She and Dr. Nath, also a member of the A.F.M. task force, said that to confirm the finding, similar studies should be run during future A.F.M. bursts, next expected in August to October of 2020. Pinpointing a specific enterovirus could lead to medications or a vaccine.
Many questions remain: Are A.F.M. cases surging every other year because of something about enteroviruses or human immunity? Why does the smattering of A.F.M. cases in off-peak years appear to have more varied causes?
And why do so few children develop A.F.M. when many are exposed to enteroviruses? Several scientists are researching possible genetic reasons. Still, even siblings, like Luca’s younger brother Mazi, who had the same cold, often don’t develop any paralysis or weakness.
Luca’s current condition is similar to many children with A.F.M., who suffer from asymmetrical bone development, muscle weakness, pain and uncoordinated movements, said Dr. Bove, now at U.C.S.F. In a recent study she co-authored about the experience of children with A.F.M., only two of 82 children were described by their parents as having completely recovered.
“He has one leg that’s shorter and skinnier than the other; he trips a lot,” Dr. Bove said. He has a “tiny, short little flimsy right arm and shoulder,” needs regular physical therapy, and during activities like running, climbing stairs or riding in the car, “he wears a neck brace because his neck is very floppy like a baby’s,” she said.