Enterovirus

Seventy-one types of enteroviruses have been discovered. Among these are Coxsackie A viruses, Coxsackie B viruses, echoviruses and polioviruses.

Enteroviral infections are usually subclinical and unlike herpesviruses, usually leave the body after an effective immune response. However, they can also cause meningitis and myocarditis, and chronic or life-threatening conditions in certain populations, such as in patients with X-linked agammaglobulinemia (XLA). Most children are exposed to at least one enterovirus by the age of 12 months.

Enteroviruses have a tropism for muscle cells and have been linked to myalgic encephalomyelitis and chronic fatigue syndrome, as well as Type 1 Diabetes.

Coxsackie B viruses
Coxsackie B (also written coxsackievirus B) is a group of six types of enterovirus, causing symptoms ranging from gastrointestinal distress to pericarditis and myocarditis. Symptoms of infection with viruses in the Coxsackie B grouping include fever, headache, sore throat, gastrointestinal distress, extreme fatigue as well as chest and muscle pain. It can also lead to spasms in arms and legs. Numerous studies have found evidence of persistent infection of Coxsackie B in the blood, muscle, gut and brain in a subset of patients with diagnosed with myalgic encephalomyelitis and chronic fatigue syndrome.

Metabolic effects
A study of poliovirus found that polio infection rapidly decreases cellular oxygen consumption (and thus energy production through cellular respiration) by inhibiting succinate dehydrogenase and blocking mitochondrial electron transport.

Role in Myalgic Encephalomyelitis
Enteroviruses, especially Coxsackie B viruses, have been posited as a key etiological factor in Myalgic Encephalomyelitis (ME) ever since the historic outbreaks of ME in the 1930s-1950s. These frequently coincided with outbreaks of polio. Findings in several outbreaks seemed to suggest that symptoms were caused by a virus distinct from but related to polio including findings of mild, diffuse peripheral nervous system damage in monkeys infected with the virus; a stronger response to polio vaccination in children who had been in epidemic areas; and seasonal patterns of infection resembling polio.

The direct evidence for enteroviral persistence in ME patients has been mixed, due in part to different methods of testing and types of tissue samples (for example muscle biopsies, stool samples, stomach biopsies, cerebrospinal fluid).

Some studies have found evidence of enteroviral infection in muscle biopsies in a subset of patients, while others have failed to replicate those results.

Research by John Chia and his son, Andrew Chia has looked for enteroviruses in gut biopsies. 82% of samples were positive for viral capsid protein 1 (VP1), compared to 20% of controls. Enteroviral RNA was detected in 37% of biopsy samples, compared to 4.7% of controls. They posit that a subset of Chronic Fatigue Syndrome patients have a chronic enteroviral infection.

Treatment
There are no FDA-approved treatments for enteroviruses. The drug Pleconaril has been shown to have activity against a number of enteroviruses    but has not been approved by the FDA.

Treatment usually involves supporting the immune response particularly in those with documented immune dysfunction. Dr. Chia treats his patients with enteroviral infection with Equilibrant, gammaglobulin and interferon.

Published Studies

 * 2016, A study on brain tissue samples from a deceased ME patient found evidence of enterovirus specific genomic sequences and enteroviral protein in the patient's cerebral cortex.
 * 2016, A study on stomach tissue samples from CFS patients found that 82% of patients have evidence of chronic enterovirus infection of the stomach.
 * 2010, A longitudinal study found that a percentage of patients presenting to emergency care with acute enterovirus infection would go on to develop symptoms of ME and CFS and had demonstrable evidence of viral persistence.
 * 1996, A Swedish study using the Fukuda criteria was unable to find evidence of any persistent enteroviral infection in fecal samples, muscle biopsies, or cerebrospinal fluid.
 * 1995, In the CFS study group, 42% patients were positive for enteroviral sequences by PCR, compared to only 9% of the comparison group.
 * 1994, A second postmortem tissue study found positive enterovirus PCR sequences in the muscle, heart, brain stem, and hypothalamus of a deceased ME patient.
 * 1990, Persistence of enteroviral RNA in chronic fatigue syndrome is associated with the abnormal production of equal amounts of positive and negative strands of enteroviral RNA. "This suggests that entrovirus pesistence in muscle is due to a defect in control of viral RNA synthesis."
 * 1990, A retrospective cohort study found that 31% of ME patients had elevated enteroviral IgM antibody levels. Sixteen of these patients were retested annually over three years and all showed persistently elevated Coxsackie B neutralizing antibody levels and intermittently positive enteroviral IgM, indicating the possibility of a persistent infection.
 * 1988, A study of 76 postviral fatigue patients and 30 controls found significantly higher numbers of positive cultures and IgM responses to enteroviruses.
 * 1988, In one study, enterovirus-specific RNA three standard deviations greater than controls was found in muscle biopsies of 20% of ME patients studied.

Talks & interviews

 * 2016, - 86. ‪ME and the role of enteroviruses / ME en de rol van enterovirussen - Dr. Byron Hyde‬, MD

Learn More

 * ME/CFS and Polio, chapter from book "ME: The New Plague", Jane Colby.