Immune responsiveness in chronic fatigue syndrome
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...
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Veröffentlicht in: | Postgraduate medical journal 1991-06, Vol.67 (788), p.532-537 |
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description | 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. |
doi_str_mv | 10.1136/pgmj.67.788.532 |
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D. ; Clements, G. B. ; Edwards, R. H.</creator><creatorcontrib>Milton, J. D. ; Clements, G. B. ; Edwards, R. H.</creatorcontrib><description>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.</description><identifier>ISSN: 0032-5473</identifier><identifier>EISSN: 1469-0756</identifier><identifier>DOI: 10.1136/pgmj.67.788.532</identifier><identifier>PMID: 1656416</identifier><language>eng</language><publisher>London: The Fellowship of Postgraduate Medicine</publisher><subject>Adolescent ; Adult ; Antibodies, Viral - analysis ; Antigen-Antibody Complex - analysis ; Biological and medical sciences ; Cell Division - immunology ; Concanavalin A - immunology ; Enterovirus B, Human - immunology ; Fatigue Syndrome, Chronic - immunology ; Female ; Humans ; Immunity ; Immunoglobulin G - analysis ; Immunoglobulin M - analysis ; Immunopathology ; Lymphocyte Activation ; Male ; Medical sciences ; Middle Aged</subject><ispartof>Postgraduate medical journal, 1991-06, Vol.67 (788), p.532-537</ispartof><rights>1992 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b490t-1715401417d14fa0dc0c79d8d7fd9dd53306254a36bb1a2b95835fdde5bbb5303</citedby><cites>FETCH-LOGICAL-b490t-1715401417d14fa0dc0c79d8d7fd9dd53306254a36bb1a2b95835fdde5bbb5303</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2398884/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2398884/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=5435671$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1656416$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Milton, J. D.</creatorcontrib><creatorcontrib>Clements, G. B.</creatorcontrib><creatorcontrib>Edwards, R. H.</creatorcontrib><title>Immune responsiveness in chronic fatigue syndrome</title><title>Postgraduate medical journal</title><addtitle>Postgrad Med J</addtitle><description>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.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Antibodies, Viral - analysis</subject><subject>Antigen-Antibody Complex - analysis</subject><subject>Biological and medical sciences</subject><subject>Cell Division - immunology</subject><subject>Concanavalin A - immunology</subject><subject>Enterovirus B, Human - immunology</subject><subject>Fatigue Syndrome, Chronic - immunology</subject><subject>Female</subject><subject>Humans</subject><subject>Immunity</subject><subject>Immunoglobulin G - analysis</subject><subject>Immunoglobulin M - analysis</subject><subject>Immunopathology</subject><subject>Lymphocyte Activation</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><issn>0032-5473</issn><issn>1469-0756</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1991</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkL1v1EAUxFcIFC6BmgrJBUqB5Ms-75fdIBELSKQIChKEaFb75csGe33s2lHy37Mnnw6oqF4xvzczGoReAV4DEH623Qx3ay7Woq7XjFRP0Aoob0osGH-KVhiTqmRUkOfoOKU7jIEICkfoCDjjFPgKweUwzMEV0aXtGJK_d8GlVPhQmNs4Bm-KTk1-M7siPQYbx8G9QM861Sf3cn9P0M3HD9ftRXn15dNl-_6q1LTBUwkCGMVAQVigncLWYCMaW1vR2cZaRgjmFaOKcK1BVbphNWGdtY5prRnB5AS9W3y3sx6cNS5MUfVyG_2g4qMclZf_KsHfys14LyvS1HVNs8Hp3iCOv2aXJjn4ZFzfq-DGOUlRAQNa75LOFtDEMaXoukMIYLlbWe5WllzIvLLMK-eP1393-8Mvs2b9zV5Xyai-iyoYnw4Yo4RxARkrF8ynyT0cZBV_5jAimPz8rZXff7TtOf1ayYvMv114nev8r-NvYfqjPA</recordid><startdate>19910601</startdate><enddate>19910601</enddate><creator>Milton, J. D.</creator><creator>Clements, G. B.</creator><creator>Edwards, R. H.</creator><general>The Fellowship of Postgraduate Medicine</general><general>BMJ</general><general>BMJ Group</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19910601</creationdate><title>Immune responsiveness in chronic fatigue syndrome</title><author>Milton, J. D. ; Clements, G. B. ; Edwards, R. H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b490t-1715401417d14fa0dc0c79d8d7fd9dd53306254a36bb1a2b95835fdde5bbb5303</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1991</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Antibodies, Viral - analysis</topic><topic>Antigen-Antibody Complex - analysis</topic><topic>Biological and medical sciences</topic><topic>Cell Division - immunology</topic><topic>Concanavalin A - immunology</topic><topic>Enterovirus B, Human - immunology</topic><topic>Fatigue Syndrome, Chronic - immunology</topic><topic>Female</topic><topic>Humans</topic><topic>Immunity</topic><topic>Immunoglobulin G - analysis</topic><topic>Immunoglobulin M - analysis</topic><topic>Immunopathology</topic><topic>Lymphocyte Activation</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Milton, J. D.</creatorcontrib><creatorcontrib>Clements, G. B.</creatorcontrib><creatorcontrib>Edwards, R. H.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Postgraduate medical journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Milton, J. D.</au><au>Clements, G. B.</au><au>Edwards, R. H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Immune responsiveness in chronic fatigue syndrome</atitle><jtitle>Postgraduate medical journal</jtitle><addtitle>Postgrad Med J</addtitle><date>1991-06-01</date><risdate>1991</risdate><volume>67</volume><issue>788</issue><spage>532</spage><epage>537</epage><pages>532-537</pages><issn>0032-5473</issn><eissn>1469-0756</eissn><abstract>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.</abstract><cop>London</cop><pub>The Fellowship of Postgraduate Medicine</pub><pmid>1656416</pmid><doi>10.1136/pgmj.67.788.532</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adolescent Adult Antibodies, Viral - analysis Antigen-Antibody Complex - analysis Biological and medical sciences Cell Division - immunology Concanavalin A - immunology Enterovirus B, Human - immunology Fatigue Syndrome, Chronic - immunology Female Humans Immunity Immunoglobulin G - analysis Immunoglobulin M - analysis Immunopathology Lymphocyte Activation Male Medical sciences Middle Aged |
title | Immune responsiveness in chronic fatigue syndrome |
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