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Industry: Email Alert RSS FeedAntiviral intervention for Chronic Fatigue Syndrome
Townsend Letter for Doctors and Patients, Feb-March, 2004 by Shari Lieberman
Chronic Fatigue Syndrome (CFS) has a long history in medical literature. In the past it has been referred to as chronic Epstein-Barr virus syndrome (EBV), chronic mononucleosis syndrome, postviral fatigue syndrome, epidemic myalgic encephalomyelitis and even "yuppie flu." In 1994 the Center for Disease Control refined the definition of CFS.
CDC, NIH and International Chronic Fatigue Syndrome Study Group Criteria for Diagnosis of Chronic Fatigue Syndrome
A case of CFS must fulfill all major criteria, plus four or more of the minor criteria. Each minor criterion must have persisted or recurred during six or more consecutive months of illness and must not have predated the fatigue. A patient who does not fully meet the CFS criteria may be given a diagnosis of idiopathic chronic fatigue.
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Major Criteria
* Unexplained, persistent or relapsing fatigue that is new or definite onset (not lifelong)
* Fatigue is not due to ongoing exertion
* Fatigue is not substantially alleviated by rest
* Fatigue easily results in substantial reduction in previous levels of occupational, educational, social, or personal activities
Minor Criteria
1. Self-reported impairment in short-term memory or concentration severe enough to cause substantial reduction in previous levels of occupational, educational, social or personal activities.
2. Sore throat
3. Tender cervical or axillary lymph nodes
4. Muscle pain
5. Multijoint pain without swelling or redness
6. Headaches of a new type, pattern or severity
7. Unrefreshing sleep
8. Postexertional malaise lasting more than 24 hours.
It has been observed that CFS occurs after a viral illness such as a severe flu. Many patients describe a relapse of an illness after which CFS occurs because more rest and a longer period of convalescence were required to recover. Initial symptoms of CFS are viral and include swollen glands, sore throat, fatigue, malaise and fever. A host of viruses has been associated with CFS including influenza, EBV, cytomegalovirus, coxsackie, polio, human herpes virus 6 (HHV-6), enteroviruses, herpes simplex 1 & 2, human T-cell lymphotropic viruses, and retrovirus. It is possible that prions and stealth viruses yet to be identified may also be involved in this illness and many may be co-infected with more than one virus. Numerous immune abnormalities have been seen in patients with CFS including decreased natural killer cell (NK) function, alterations in interferons (INF), interleukins and other cytokines and tumor necrosis factor (TNF).
To date there are no safe and effective antiviral drugs to treat CFS. However, there are many natural compounds that are safe and effective and have broad antiviral action, many of which also modulate immune function to fight viruses. Additionally, some of these compounds have the added benefit of antifungal and antibacterial activity. Chronic immune suppression often results in candidiasis (Candida albicans infection) which can cause further immunosuppression.
Glycyrrhizin
Glycyrrhizin (GL) is one of the active antiviral compounds found in licorice root (Glyrrhiza glabra). It has been used in Japan as an intravenous drug for more than 20 years as Stronger Neo-Minophagen C (SNMC) and research has shown it to be extremely effective for hepatitis (A, B, C), HIV, cancer and many other serious viral illnesses. Licorice is in many Kampo medicines (Japanese Herbal Medicine) for immune modulation and antiviral therapy. GL is absorbed orally. GL is a conjugate of glycyrrhetinic acid (GA) and glucuronic acid. Oral GL is metabolized in the intestine to GA and both are active antiviral compounds. Intravenous GL is metabolized into GA when excreted through the bile into the intestines. GL and GA exhibit similar properties. Both have been shown to be effective for hepatitis A, B, C; Human Immunodeficiency virus (HIV); Herpes (I, II, Zoster, perhaps HHV-6); lichen planus, influenza, cytomegalovirus (CMV), cancer, phlebovirus and vaccinia virus. GL/GA increases the effectiveness of INF therapy in patients with hepatitis C. GL/GA also modulates cortisol levels which are often abnormal in patients with CFS. These compounds improve immunocompetence and reduce susceptibility to candida albicans. GL/GA are antibacterial to H. pylori and klebsiella pneumoniae.
GL/GA have direct antiviral activity and can inhibit some RNA transcriptases (HIV). They also have an indirect antiviral action and can decrease cell membrane permeability (e.g. decrease hepatocyte injury in hepatitis); inactivate viruses and inhibit viral proliferation. Both compounds are also potent antioxidants and free radical scavengers and protect normal, healthy cells from injury. GL/GA can increase gamma interferon, T cells, NK cells and improve immune function. They also selectively inhibit cytolytic reactivity of the complement system. However, these compounds do not inhibit (may enhance) immune adherence responsible for immune phagocytosis, regulation of antibody production in protective immunity against invaders. GL/GA also inhibits the arachidonic acid cascade (phospholipase A2) thereby reducing inflammation.