Viral onset hypothesis

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The Viral onset hypothesis is a prominent theory as more than half of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) patients report falling ill after an acute viral infection.[1] Many different viruses have been researched as possible etiological agents.[1]

Disease onset[edit | edit source]

Some think there is a single, novel viral agent as yet undiscovered.

Others think many different viruses can initiate and sustain the disease. Viruses linked to disease onset include herpesviruses such as Epstein-Barr virus or HHV-6, enteroviruses such as coxsackie or even influenza (the flu) or a flu-like illness.[1] Many viruses and pathogens have been investigated, with finding being mixed and no particular pathogen found.[1]

There are several hypotheses for how the viral trigger initiates and perpetuates the disease.

Evidence[edit | edit source]

Viral Onset Hypothesis in ME. Viral involvement is supported by an infectious initiating trigger in at least half of the patients (21), and by confirmed findings of biochemical dysregulation of the 2-5A synthetase/ribonuclease L (RNase L) antiviral defense pathway in monocytes (22,23,24,25,26), a pathway which is activated in viral disorders (27). - Canadian Consensus Criteria
Some evidence has exists supporting the viral onset hypothesis, but no pathogen has been identified yet.

Chronic infection[edit | edit source]

Some think that there may be a low grade, chronic infection whereby the initial virus continues to provoke an immune response, especially in key areas such as the gastrointestinal tract, muscle, and the brain, brain stem, and spinal cord.

Autoimmune disease[edit | edit source]

Some think that symptoms are caused by an inflammatory process that is triggered by an initial infection and continues even after the initial virus is no longer replicating. It is possible that ME/CFS is an autoimmune response that can be triggered by many different infections.

Viral reactivation[edit | edit source]

Still others think that an immune deficiency allows otherwise common or benign viruses to replicate.

Dysbiosis[edit | edit source]

Viral infection may trigger dysbiosis leading to alterations in the immune system and gut-brain axis and causing the symptoms of the disease.

Outbreaks[edit | edit source]

There have been dozens of reported clusters and outbreaks of ME, which all suggest a role of either a communicable pathogen or in some cases, a toxic agent.

See also[edit | edit source]

References[edit | edit source]

etiology The cause of origin, especially of a disease.

myalgic encephalomyelitis (ME) - A disease often marked by neurological symptoms, but fatigue is sometimes a symptom as well. Some diagnostic criteria distinguish it from chronic fatigue syndrome, while other diagnostic criteria consider it to be a synonym for chronic fatigue syndrome. A defining characteristic of ME is post-exertional malaise (PEM), or post-exertional neuroimmune exhaustion (PENE), which is a notable exacerbation of symptoms brought on by small exertions. PEM can last for days or weeks. Symptoms can include cognitive impairments, muscle pain (myalgia), trouble remaining upright (orthostatic intolerance), sleep abnormalities, and gastro-intestinal impairments, among others. An estimated 25% of those suffering from ME are housebound or bedbound. The World Health Organization (WHO) classifies ME as a neurological disease.

The information provided at this site is not intended to diagnose or treat any illness.
From MEpedia, a crowd-sourced encyclopedia of ME and CFS science and history.