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Tuesday 3 September 2019
Enterovirus D68 – The New Polio?

This week WAidid suggests the article Enterovirus D68 – The New Polio?, recently published on "US National Library of Medicine- National Institutes of Health".


Enterovirus D68 (EV-D68) is a single-stranded positive-sense RNA virus of the Picornaviridae family, belonging to the species EV D, first isolated from respiratory samples in 1962 in California, from four pediatric patients with acute respiratory symptoms. EV-D68 is classified into three genetic clades, A, B and C; subclades A1, A2, B1, and B2 can be further identified depending on EV typing, targeting either VP1 or VP4-2 capsid protein. EV are transmitted via the fecal-oral route and replicate in the intestine. EV are thought to have existed and coevolved with humanity for thousands of years. The causative agent of poliomyelitis (poliovirus), was not discovered until 1908: it was not only the first EV to be discovered, but also caused the most devastating and widespread morbidity and mortality of all the EV genotypes. Over the subsequent years, over 100 EV serotypes have now been discovered with nearly 70 species infecting humans. Non-polio EV can cause a variety of clinical syndromes, ranging from hand-foot and mouth disease to aseptic meningitis.

The introduction of the poliovirus vaccine (inactivated injectable vaccine, developed by Jonas Salk in 1955, and orally vaccine developed by Albert Sabin in 1961), dramatically reduced the incidence of infections globally, with only small clusters sporadically occurring. According to the Global Poliovirus Eradication Initiative (GPEI), only Afghanistan and Pakistan still report endemic wildtype poliovirus in 2018 and only few new cases of vaccine-derived poliovirus in the Democratic Republic of the Congo, Nigeria, Somalia and Papua New Guinea have been reported. Therefore, cases of acute flaccid paralysis (AFP) outside these countries have decreased to very low numbers.

EV-D68 had only been reported sporadically worldwide since 2010. Indeed before 2014, only sporadic outbreaks were reported, but it rapidly became an emerging neuropathogenic threat. Specific testing for EV-D68 or routine typing for EV are not standard practice in the majority of laboratories, so the true burden of disease is not known.

The authors reported the details about the 2014 outbreak in United States and Canada and the 2016 outbreak in the Netherlands.

Depending on the clinical picture, several diagnostic samples can and should be collected to detect EV: cerebral spinal fluid (CSF), feces, respiratory material and serum/plasma. Molecular testing (RT-PCR targeting the 5’UTR) is recognized as the gold standard for diagnosing an EV infection. Sanger sequencing of the VP1, and occasionally VP4-2 structural proteins, is considered the gold standard for the determination of specific EV genotype. Next generation sequencing (NGS) allows useful information about changes in tropism or pathogenicity of EV.

The authors reviewed the data about the connection between EV-68 and acute flaccid myelitis (AFM), reporting case definition, use of magnetic resonance in the diagnosis, and highlighting the present lack of the exact pathogenetic mechanism through which EV-D68 instigates infection.

The authors concluded reporting the most important gaps in the EV-D68 management: absence of vaccine and effective treatment (although reporting the most promising therapies, such as 8V-7404, DAS181, Rupintrivir, nerve and muscle transfer), lack of a specific surveillance system, and the necessity of a routinely use of NGS.

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AUTHORS: Cassidy H., Poelman R., Knoester M., Van Leer-Buter C., Niesters H.