Enterovirus D68 (EV-D68) has been accused of playing a key role in paralytic disease that has affected hundreds in the United States in recent years. Unfortunately, so far, evidence of his presence has been at best a circumstance.
Finally, the researchers found signs of the fingerprint of the virus exactly where it matters: in the spinal fluid of patients affected by poliomyelitis. It still does not tell us how the condition arises, but having such solid evidence of the alleged cause is a significant step in the right direction.
Two recent additional studies have identified the presence of enterovirus-specific antibodies in a fluid surrounding the central nervous system of patients diagnosed with acute myelitis or AFM.
A study published in August found sparse signs of virus RNA in patient serum and spinal fluid samples, but identified enterovirus antibodies in nearly 80 percent of AFM cases, compared with only 20 percent of healthy patients.
The results are certainly impressive, but the small size of the study is considered; an incomparable sample of only 1
Now, a more recent study conducted by researchers at the University of California San Francisco found similar results among 42 children diagnosed with AFM.
By exposing fluid samples in a library of just under half a million viral proteins, researchers continued to search for antibodies in the patient's spine that could recognize the enterovirus.
These samples were compared with samples taken from 58 children who were healthy or had other different neurological conditions.
Like the previous study, there are few signs of the virus itself. But in over two-thirds of the samples from patients with AFM, antibodies were found corresponding to proteins belonging to the virus family and the genus EV-D68. In comparison, only 7 percent of controls presented with similar antibodies in their spinal fluid.
Further testing using a separate, more sensitive test confirmed it – virus antibodies are far more likely to be present in the nervous system of patients with paralyzing conditions.
The results are insufficient to capture the virus with red hands, but still provide the strongest evidence to date that the relatively common pathogen is behind an epidemic that has plagued health authorities for years.
AFS cases have grown every two years since it was first recognized in 2012, with hundreds of children in the US suffering from the disabling effects of the disease.
Symptoms usually start very much like a cold, but can progress steadily to severe neurological damage that weakens muscles and reduces reflex movement.
The similarities with the paralyzing effects of polio initially attract comparisons between diseases, but without the signs of poliovirus found in anyone diagnosed with AFS, epidemiologists should look elsewhere.
The focus soon turned to EV-D68, a relatively common pathogen ever associated with mild respiratory problems.
The agent was not exactly unknown to health experts, which was first identified in the 1960s, but was also not considered a cause of concern, with only 26 cases of infection reported in the United States with EV-D68 from 1970 to 2005.
This changed in 2014, with reports of record outbreaks of severe respiratory infections caused by EV-D68 in the United States.
Overlap in the foci between AFS and EV-D68, not to mention the fact that many diagnosed with wi AFS report having symptoms similar to colds and muscle fatigue, and it seems likely that the two are related.
In 2017, researchers demonstrated that the virus was capable of causing paralysis in mice. It looked like an open and closed case.
But no one can find convincing signs of the actual virus in people with AFS. Without any way of putting the virus in place in any case, there will always be doubt.
"People have been imprisoned by the fact that enteroviruses are rarely detected in the cerebrospinal fluid of AFM patients," says UCSF neurologist Michael Wilson.
"They wanted to know how someone could get neurological symptoms without detecting a virus in their central nervous system."
With matching fingerprints in the form of antibodies, though researchers can now redouble their efforts to understand the underlying pathology of this once wicked virus and maybe even explain how it turned out so bad.
There is currently no specific way to prevent AFS. Fortunately, it is estimated that less than one in one hundred children infected with EV-D68 are susceptible to the paralyzing effects of AFM. Learning why this is another conundrum and one that future research can hopefully solve.
This study was published in by Nature Medicine .