Serological and metagenomic interrogation of cerebrospinal fluid implicates enteroviruses 2 in pediatric acute flaccid myelitis (2019) Schubert et al

[JohnTheJack]

Preprint made available here.

https://www.biorxiv.org/content/biorxiv/early/2019/06/10/666230.full.pdf

Conclusion
Despite the rare detection of EV RNA in the CNS of patients with AFM, our pan-viral serologic assay identified high levels of CSF EV antibodies in AFM CSF compared to CSF from OND controls. These results provide further evidence for a causal role of non-polio enteroviruses in AFM.

 

[Andy]

I think this is now published as

Pan-viral serology implicates enteroviruses in acute flaccid myelitis

Abstract
Since 2012, the United States of America has experienced a biennial spike in pediatric acute flaccid myelitis (AFM)1,2,3,4,5,6. Epidemiologic evidence suggests non-polio enteroviruses (EVs) are a potential etiology, yet EV RNA is rarely detected in cerebrospinal fluid (CSF)2. CSF from children with AFM (n = 42) and other pediatric neurologic disease controls (n = 58) were investigated for intrathecal antiviral antibodies, using a phage display library expressing 481,966 overlapping peptides derived from all known vertebrate and arboviruses (VirScan). Metagenomic next-generation sequencing (mNGS) of AFM CSF RNA (n = 20 cases) was also performed, both unbiased sequencing and with targeted enrichment for EVs. Using VirScan, the viral family significantly enriched by the CSF of AFM cases relative to controls was Picornaviridae, with the most enriched Picornaviridae peptides belonging to the genus Enterovirus (n = 29/42 cases versus 4/58 controls). EV VP1 ELISA confirmed this finding (n = 22/26 cases versus 7/50 controls). mNGS did not detect additional EV RNA. Despite rare detection of EV RNA, pan-viral serology frequently identified high levels of CSF EV-specific antibodies in AFM compared with controls, providing further evidence for a causal role of non-polio EVs in AFM.

Paywall, https://www.nature.com/articles/s41591-019-0613-1
Not currently available via Scihub

Article about this and another recent study, https://www.sciencemag.org/news/2019/10/evidence-links-poliolike-disease-children-common-type-virus

 

[InitialConditions]

https://www.ucsf.edu/news/2019/10/4...HAsSPsa2ynYLfKVUTWfyXryLHq03HmMv-bPQ2ZVwkYsP4

 

[InitialConditions]

Are there studies of searches for enteroviruses in the CSF of M.E. patients?

 

[Saz94]

https://medicalxpress.com/news/2019...yzed-polio-like.amp?__twitter_impression=true

 

[Saz94]

Do these findings make it more likely that an enterovirus may be involved in ME too?

 

[Jonathan Edwards]

Do these findings make it more likely that an enterovirus may be involved in ME too?

I don't think so. If anything they emphasise how clinically different ME is from enteroviral infections.

 

[Saz94]

I don't think so. If anything they emphasise how clinically different ME is from enteroviral infections.

Thanks, can you expand on that please?

 

[Jonathan Edwards]

Thanks, can you expand on that please?

Enteroviral infections like polio and this one produce permanent local nerve cell damage with corresponding clinical signs from a one off episode. ME does not produce local nerve cell damage as far as we know and the illness is chronic and fluctuating. There really is no similarity as far as I can see.

I think the whole discussion about ME and enteroviruses comes from the confusion raised by Acheson and others who muddled an acute epidemic that might or might not have been associated with focal neurological lesions and a chronic illness that followed in some case. Even if we think ME in recent times is in some cases precipitated by viral infections the acute illness and ME are completely different problems.