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Query: UMLS:C0015674 (chronic fatigue syndrome)
 2,978 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic fatigue syndrome (CFS) is characterized by unexplained, debilitating fatigue or easy fatigability lasting longer than six months. While a viral basis of infection is proposed to be the cause of CFS, other viral infections do not generally persist after several weeks. Immunological disorders, including abnormal functions and distributions of T lymphocytes, B lymphocytes, natural killer (NK) cells, and monocyte/macrophages, are described in CFS. NK cells are known to play an important role in host resistance against viral infection as well as in the regulation of the immune systems. Restoration of NK activity resulted in recovery from CFS. Taken together, immunological abnormalities, especially dysfunction of NK cells, may be involved in CFS.
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PMID:[Chronic fatigue immune dysfunction syndrome]. 128 38

Chronic fatigue syndrome (CFS) is newly-recognized disease characterized by chronic and debilitating fatigue. It has been suggested that viral infection may be involved in this syndrome from the results of clinical examination, including increased activity of 2',5'-synthetase in leukocytes of patients. The following viruses have been reported as etiologic agents of this disease. First, many studies have found elevated levels of IgG to viral capsid antigen and early antigens to Epstein-Barr virus (EBV), but low titer or absence of antibody to EBV-associated nuclear antigen. Second, the enteroviruses have also been implicated as possible causative agent of CFS, because virus could be isolated from patients. Recently it was also reported that antibodies to human T-lymphotropic virus (HTLV) and HTLV type II (HTLV-II) gag sequence were detectable in patients. Finally several reports state that human herpesvirus 6 (HHV-6) could be isolated from CFS patients in the high frequency. In conclusion, it is still early to identify the etiologic agent from these reports, and more effort is needed.
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PMID:[Chronic fatigue syndrome and virus infection: human herpesvirus 6 (HHV-6) infection]. 133 58

Patients with chronic fatigue syndrome (CFS), of unknown etiology, have been increasingly reported. This syndrome is characterized by debilitating fatigue, lymphadenopathy, and fever. Herein, I focus on and review this syndrome from the view point of the causative role of viral infection. Since the symptoms of CFS are similar to those of chronic infectious mononucleosis (CIM) or chronic Epstein-Barr virus infection (CEBV), the role of EBV has been intensively studied. The etiological relationship between EBV and CFS, however, is questioned, like other lymphotropic viruses, including human retroviruses, adenoviruses and human herpesvirus 6. Additionally, severe chronic active EBV infection syndrome (SCAEBV) is also discussed in this review because symptoms of this disorder are similar to those of CFS but more severe in degree. Currently, the cause(s) and treatment of CFS are enigmatic and require further research and multidisciplinary study.
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PMID:[Viral infection and its causative role for chronic fatigue syndrome]. 133 59

The chronic fatigue syndrome (CFS) is a poorly understood condition with nonspecific signs and symptoms, especially debilitating fatigue. Most patients can pinpoint the onset of their illness and usually describe a flu-like state. The search for an etiologic agent has focused on a number of viruses such as Epstein-Barr, enteroviruses, retroviruses, and human herpesvirus-6. Evidence supports persistent viral infection in a small percentage of CFS patients. Immunologic abnormalities do exist in CFS, which indicate the presence of immune activation in CFS patients. Although abnormal muscle biopsies have been found in some patients with CFS, strength and endurance appear normal, but perception of exertion may be abnormal. Patients with chronic fatigue have a high incidence of premorbid and concurrent psychiatric disorders, and on physical examination many often have reproducible tender points similar to fibromyalgic patients. Clinical evaluation should rule out other potential causes of fatigue, but elaborate diagnostic tests are seldom required. Presently, no specific treatment exists for CFS. A cognitive behavioral approach with or without the use of tricyclics has been advocated. Patients should be encouraged to maintain functional status and should not be discouraged from exercise. Several medications have been tried but with no definite clinical benefit.
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PMID:Chronic fatigue syndrome. 161 43

The prevalence and activity of human herpesvirus-6 in patients with collagen vascular diseases (CVD) was determined. One hundred and fifty patients with CVD (56 with systemic lupus erythematosus-SLE, 92 with rheumatoid arthritis-RA, 1 with Sharp's syndrome and 1 with atypical polyclonal lymphoproliferation-APL and rheumatoid features) were screened serologically (IFA and ELISA) for antibodies against human herpesvirus-6 (HHV-6), Epstein-Barr virus (EBV) and cytomegalovirus (CMV). Virus isolation was attempted from peripheral blood lymphocytes (PBL) of 25 persons with various disorders. PBL were grown in tissue culture and tested with standard HHV-6-positive antisera for viral antigen expression. Supernatants of the patient's lymphocyte cultures were used to infect HSB2 cells, and virus infection in these cells was proven by IFA, in situ hybridization and by electron microscopy. Fifty-five percent of the SLE patients, 6.5% of the RA patients and both patients with Sharp's syndrome or with APL had antibody titers indicative of active HHV-6 infection. Virus cultures were positive in 9 of the 25 attempts with establishment of stable virus lines. These patients were 5 with SLE or UCVD, and one each with RA, CFS, APL as well as one healthy control. Reactivated and chronic active HHV-6 infections are frequent in SLE like EBV in RA. The role of these viruses in the pathogenesis of the diseases or in their reactivation still needs further investigation.
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PMID:Isolation of human herpesvirus-6 (HHV-6) from patients with collagen vascular diseases. 165 47

We have endeavoured to find immunological indications of chronic virus infection in patients with chronic fatigue syndrome (myalgic encephalomyelitis) and to investigate immune responsiveness to viruses in such patients in comparison with normal subjects and patients with muscular dystrophy. Levels of circulating IgM immune complexes were elevated (above the 95% normal control range) in 10 (17%) of 58 patients with chronic fatigue syndrome, which was not significantly different from the normal controls or from dystrophy controls (by Mann Whitney U test). Levels of IgG complexes were only increased in 10% of patients. Lymphocyte proliferation in response to concanavalin A (Con A), assessed by increase in 3H-thymidine incorporation, did not differ between 14 patients and 18 normal subjects. The proliferative response to Coxsackie B virus antigen did not differ between chronic fatigue patients and normal subjects when expressed either as an increase in counts or as a stimulation index. Adjustment of the counts in relation to the proliferation response to Con A, as an indication of the overall proliferative response of the cell preparation, did not reveal any hidden difference. IgM antibodies to Coxsackie B viruses were not found in any of 20 patients and in 1 of 20 dystrophy controls. Significant levels of neutralizing antibodies to Coxsackie B viruses 1-5 were found in 6 out of 19 (32%) patients compared with 4 out of 17 (24%) dystrophy controls, which does not differ from currently expected normal incidence. Antibody titres to other respiratory viruses were also not notably different between the patient and control groups. In conclusion we can find no evidence for a definable viral aetiology for the chronic fatigue syndrome, neither in terms of a persistent infection nor an altered ability to respond to virus.
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PMID:Immune responsiveness in chronic fatigue syndrome. 156 Nov 98

Nucleic acid was extracted from muscle biopsy samples from a series of highly selected patients suffering from chronic muscle fatiguability following a viral infection (Postviral Fatigue Syndrome: PVFS). Samples were examined for the presence of enteroviral RNA sequences or Epstein-Barr (EBV) virus DNA sequences by molecular hybridisation as these two agents have been implicated by retrospective serology in the aetiology of PVFS. We found enteroviral RNA in 24% of biopsy samples and EBV DNA in a further 9% of biopsy samples: no biopsy was positive for both enteroviral RNA and EBV DNA. In addition, in the case of enteroviruses we found that the persisting virus is defective in control of RNA replication as both strands of enteroviral RNA are present in similar amounts: this is unlike the asymmetric synthesis of genomic RNA seen in a productive, cytolytic enterovirus infection. The implications of these data in relation to mechanisms of viral persistence and muscle dysfunction are discussed.
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PMID:Persistent virus infection of muscle in postviral fatigue syndrome. 166 79

The etiologic bases of CFS are undetermined at the present time. It is very important to distinguish the patients with CFS as defined by the Centers for Disease Control (CDC) case definition of Holmes et al. from patients with physical and laboratory findings suggesting dual infections and/or underlying immunodeficiency. Particularly fruitful might be a longitudinal immunovirologic study of patients who exhibit CFS following a well-documented viral infection.
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PMID:Dual infections of the immune system in patients with chronic active Epstein-Barr virus infection mimicking chronic fatigue syndrome. 166 50

Postviral fatigue syndrome is associated with persistent infection by a virus. The patient with the condition has failed to eliminate the virus in the usual time. There is little evidence of a deficient immune response by the patient as the explanation for the viral persistence, and it must be assumed that most of the explanation lies in down-regulation of virus expression in infected cells. The general symptomatology of postinfectious syndromes may be mediated by cytokines liberated as part of the infection. Part of the syndrome may also be due to local effects of virus infection in muscles or the central nervous system (CNS).
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PMID:Immunology of postviral fatigue syndrome. 172 5

This chapter reviews the evidence concerning the importance of psychological and social factors in the aetiology and pathogenesis of chronic fatigue syndrome. The diagnosis is often offered to doctors by patients; and we consider attribution, stigma, collusion between doctor and patient, and abnormal illness behaviour in this context. We then give a brief description of a model for common mental disorders, and show how chronic fatigue syndrome relates to this model. It emerges that there are special vulnerability factors in these patients' personalities before the viral illness, but the disorder is seen as being released by the viral illness. By the time the disorder becomes established the original causal nexus is seen as no longer so important, and the disorder can be seen as a form of abnormal illness behaviour maintained by special factors. The implications for treatment are then considered.
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PMID:Psychiatric perspectives: an overview. 179 90


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