Paul Has Measles is a children's book about viruses and vaccines available in English (download pdf) Spanish (download pdf) French (download pdf) German (download link) Portuguese (download pdf) Romanian (download pdf), Italian (download pdf), Croatian (download pdf) Mixtec (download pdf) Hindi (download pdf) Russian (download pdf) Japanese (download pdf) and Nahuatl (download pdf). Kindle and paperback versions also available at Amazon in English, Spanish, French.

EV-D68The Centers for Disease Control and Prevention thinks that viruses play a role in the childhood paralysis called acute flaccid myelitis (AFM). The finding of antibodies to enterovirus D68 (EV-D68) in the cerebrospinal fluid of patients with AFM strengthens the link between infection with this virus and AFM.

Acute flaccid myelitis (AFM), which mainly occurs in children, involves weakness of the arms and legs and may include other symptoms such as inability to breathe or swallow. There have been outbreaks of AFM in the US in 2014, 2016, and 2018, mainly in the late summer and early fall. The outbreaks of AFM are associated with infection with enteroviruses.

AFM was first defined in 2014 after reports of limb weakness in children across the US during an outbreak of respiratory disease caused by EV-D68 (pictured). AFM may also be associated with infections caused by other viruses, such as enterovirus A71, Coxsackievirus A16, West Nile virus and adenovirus.

Of the 233 patients with confirmed AFM in 2018, EV-D68 was the most frequently detected virus, mainly in respiratory samples. Confirming a viral etiological agent of AFM would be greatly strengthened by finding virus in the cerebrospinal fluid (CSF). However in 2018 only two samples of cerebrospinal fluid from AFM patients were found to be positive for viral RNA: one for EV-D68 and one for EV-A71. There may be multiple reasons for the failure to detect viral RNA in CSF, including clearance of virus by the time AFM is diagnosed, or very low levels of viral genomes.

An alternative to searching for viral genomes in CSF is to identify anti-viral antibodies, which may be produced during infection of the brain and spinal cord. Peptide microarrays were used to detect antibodies against enteroviruses in CSF of AFM patients. In this method, 160,000 unique peptides from the capsid proteins of all known human enteroviruses were spotted on slides. CSF samples were incubated with the slides and binding of antibodies to peptides was quantified. The results revealed antibodies to an 18 amino acid peptide of capsid protein VP1 in serum and CSF of 11/14 AFM patients and 3/26 controls. This amino acid sequence is known to be conserved among diverse human enteroviruses.

More importantly, antibodies to a 22 amino acid sequence in VP1 of EV-D68 were identified in CSF of 6/14 AFM, and in 8/11 serum samples. No immunoreactivity to this peptide was detected in samples from 26 controls.

Detection of antibodies in the CSF is not diagnostic of CNS infection because antibodies are known to pass from blood to CSF. The normal ratio of antibodies in blood to CSF is 250:1. Consequently, for diagnostic purposes, both serum and CSF should be analyzed for the presence of antibodies.

The authors of the study acknowledge this issue, noting that they do not have sufficient simultaneously collected serum and CSF samples to exclude that antibodies they detected in the CSF simply came from the blood. They note that of the 16 control patients with serum antibodies to enteroviruses, only 3 also had such antibodies in CSF. Furthermore, in a study of unexplained encephalitis in India, of 77 children with serum antibodies to enteroviruses, only 3 also had EV antibodies in CSF. For these reasons the authors do not believe that the anti-EV-D68 antibodies they have detected in CSF have come from the blood.

How can it be definitively proven that EV-D68 causes AFM? With an outbreak of AFM expected in the late summer of 2020, there should be ample opportunity to obtain numerous clinical samples – nasopharyngeal wash, serum and CSF – to examine for the presence of EV-D68 antibodies and viral genomes.

By David Tuller, DrPH

People who know little or nothing about the illness or cluster of illnesses variously called myalgic encephalomyelitis, chronic fatigue syndrome, CFS/ME, and ME/CFS can’t seem to stop writing stupid and ill-informed stories about it. And Professor Michael Sharpe seems to blame “Americans”–rather than his own disastrous research–for his current problems and the reputational damage he has suffered. That’s mainly what I got from articles in The Guardian and Psychology Today that followed one another in quick and dispiriting succession last month.

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From the meeting of the Centers of Excellence for Influenza Research and Surveillance, Vincent speaks with Alan, Florian and Jennifer about their careers, the purpose of CEIRS, universal influenza vaccines, and cellular responses to infection in pediatric populations.

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RNA recombinationRNA viruses exist close to their error threshold, the point beyond which additional mutations cause loss of infectivity. It has been suggested that RNA recombination prevents viruses from exceeding the error threshold – a situation called error catastrophe – but there has been little experimental support for this hypothesis. An analysis of poliovirus RNA synthesis suggests that this hypothesis is correct.

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The complete TWiV team give a report on the Ebola virus outbreak in DRC, and reveal that cell surface nectin proteins cause the transfer of cytoplasmic cargo, including measles virus, between cells.

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Viruses and autoimmunity

by Gertrud U. Rey

Type 1 diabetes is an organ-specific autoimmune disease that is characterized by the loss of insulin-producing beta cells in the pancreas. The loss of these cells leads to decreased insulin production (hypoinsulinemia) and increased levels of glucose in the blood (hyperglycemia). While it is still unclear what exactly causes the loss of beta cells, experts agree that it is likely a combination of genetic and environmental factors. An increasing body of evidence suggests that Coxsackievirus strain B4 is an environmental trigger, because it specifically targets beta cells, causing them to die.

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By David Tuller, DrPH

Some Australian members of the GET/CBT ideological brigades have published yet more nonsense and drivel about “graded exercise therapy” as a treatment for ME/CFS, or what they are still calling “chronic fatigue syndrome.” The article, simply called “Chronic fatigue syndrome: graded exercise therapy,” is in a peer-reviewed journal from a reputable publisher yet is full of unsupported and questionable claims. It references the PACE trial without discussing the developments that have undermined the trial’s credibility, including published re-analyses that refute the core findings. In fact, it reads as if the authors are unaware that the entire debate has been transformed in recent years–which isn’t surprising, because it is basically a reprise of material created in 2015 by the Royal Australian College of General Practitioners.

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From ASV 2019 at the University of Minnesota, TWiV explores the origins of the American Society for Virology with Sid Grossberg and Pat Spear.

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Most contemporary virologists use the term replication to indicate either the production of new virus particles or viral genomes. Because these are very different processes, during the preparation of the fourth edition of the textbook Principles of Virology, the authors decided to use the word reproduction to designate the production of new infectious virus particles, and replication when referring to nucleic acid synthesis. Recently I learned from Bill Summers, speaking at ASV 2019, how the historical use of these two words reflects our evolving concept of virus.

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From the European Congress of Virology in Rotterdam, Vincent and local co-host Ben Berkhout speak with Ron Fouchier, Rosina Girones, and Marie-Paule Kieny about their careers and their work on influenza virus, environmental virology, and developing an Ebola virus vaccine during an epidemic.

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Show notes at microbe.tv/twiv