Evaluation of autoantibodies to common and neuronal cell antigens in Chronic Fatigue Syndrome
Suzanne D Vernon and William C Reeves
Journal of Autoimmune Diseases 2005, 2:5doi:10.1186/1740-2557-2-5
People with chronic fatigue syndrome (CFS) suffer from multiple symptoms including fatigue, impaired memory and concentration, unrefreshing sleep and musculoskeletal pain. The exact causes of CFS is autoimmune, but the symptom complex resembles that of several diseases that affect the immune system and autoantibodies may provide clues to the various etiologies of CFS. We used ELISA, immunoblot and commercially available assays to test serum from subjects enrolled in a physician-based surveillance study conducted in Atlanta, Georgia and a population-based study in Wichita, Kansas for a number of common autoantibodies and antibodies to neuron specific antigens. Subsets of those with CFS had higher rates of antibodies to microtubule-associated protein 2 (MAP2) (p = 0.03) and ssDNA (p = 0.04). There was no evidence of higher rates for several common nuclear and cellular antigens in people with CFS. Autoantibodies to specific host cell antigens may be a useful approach for identifying subsets of people with CFS, identify biomarkers, and provide clues to CFS etiologies.
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Successful Intravenous Immunoglobulin Therapy in 3 Cases of Parvovirus B19-Associated Chronic Fatigue Syndrome
Three cases of chronic fatigue syndrome (CFS) that followed acute parvovirus B19 infection were treated with a 5-day course of intravenous immunoglobulin (IVIG; 400 mg/kg per day), the only specific treatment for parvovirus B19 infection. We examined the influence of IVIG treatment on the production of cytokines and chemokines in individuals with CFS due to parvovirus B19. IVIG therapy led to clearance of parvovirus B19 viremia, resolution of symptoms, and improvement in physical and functional ability in all patients, as well as resolution of cytokine dysregulation.
Chronic fatigue syndrome (CFS) is characterized by severe debilitating fatigue that persists for 6 months and is accompanied by 4 of the following symptoms: impaired memory or concentration, sore throat, tender cervical or axillary lymph nodes, muscle pain, multijoint pain, new headaches, unrefreshing sleep, and postexertional malaise .
Although the causes of and risk factors for CFS are not well defined, epidemiological studies reveal that flulike illnesses suggestive of infective episodes precede the onset in the majority of cases. A major hypothesis for the pathogenesis of CFS is that an infectious trigger, such as the persistence of an infectious agent or other immune stimulus, may lead to a chronic activation of the immune system with abnormal regulation of cytokine production . The resulting dysregulation in cytokine pathways may directly or indirectly contribute to the symptom complex associated with this disorder.
We have previously shown that acute symptomatic parvovirus B19 infection is associated with elevated circulating TNF- and IFN- production  and with particular human leukocyte antigen class 1 and 2 alleles , and it may be followed by the development of CFS [8, 9]. Persistent parvovirus B19 infection is believed to result from a deficiency in the humoral immune response to this virus .
Intravenous immunoglobulin (IVIG) therapy has been shown to be effective for parvovirus B19associated pure RBC aplasia in immunosuppressed persons  and also for several cases of other clinical manifestations in association with persistent parvovirus B19 infection, including 1 case of parvovirus B19-associated CFS .
The purpose of this study was to determine whether IVIG therapy could ameliorate the clinical symptoms and reverse the documented dysregulation in cytokine production in 3 cases of parvovirus B19-associated CFS.
Case reports. The patients are numbered 2, 8 and 32, as reported elsewhere [8, 9].
Patient 2, as described elsewhere , was a 42-year-old white woman who initially presented with an illness characterized by fever, skin rash, polyarthralgia, and fatigue coincident with an outbreak of parvovirus B19 infection at the school attended by her children.
After a 5-month history of symptoms, she was tested in March 1998 and found to be positive for serum antiparvovirus B19 IgM. This patient also reported a deterioration in memory and concentration, sore throat, painful aching muscles, new headaches, difficulty sleeping, unrefreshing sleep, postexertional malaise, an increased tendency to sweat, dizzy spells, and blurred vision. She had also experienced a sensation of heat in the soles of her feet and hot, dry eyes.