Coxsackie B Neutralisation Titres in Polymyositis/Dermatomyositis

Travers, Richard; Hughes, G. R. V.; Cambridge, G; Sewell, J. R.

doi:10.1016/s0140-6736(77)92487-4

Cited by 73 publications

(19 citation statements)

References 10 publications

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“…In 1 child with chronic myositis, CVB2 was isolated from the stool, and a rise in the titer of complement-fixing antibody was documented (26), which is similar to reports of increases in complement-fixing B4 antibodies in active juvenile DM (27). Sera from newly diagnosed children from the Chicago area in the time period 1974-1980 had an increased frequency of antibody (both neutralizing and complement-fixing) to CVB (5), which was not reproduced by the same group of investigators in a study of 20 children with juvenile DM from the same region with onset of disease in the years 1987-1992 (18), suggesting either antigenic variation or that antibodies to picornavirus are irrelevant to disease pathogenesis in juvenile DM.…”

Section: Discussionsupporting

confidence: 78%

“…There was no difference in the frequency of the presence of (P = 0.002). (25) 13 (18) 14 (19) 17 (23) 5169 (7) 28170 (40) 0169 ( 0 ) i 18 (25) 29 (50) 23 (51) 14 (64) 23 (40) 16 (36) 9 (41) 17 (29) 15 (33) 8 (36) 10 (17) 4 (9) 7 (32) 17 (29) 12 (27) 7 (32) 22 (38) 17 (38) 9 (41) 3 (5) 26159 (44) 3 (5) * Control group consisted of healthy children and children with juvenile rheumatoid arthritis (JRA).…”

Section: Demographic Characteristics Of the Study Groupsmentioning

confidence: 99%

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New‐onset juvenile dermatomyositis. Comparisons with a healthy cohort and children with juvenile rheumatoid arthritis

Pachman

Hayford

Hochberg

et al. 1997

Arthritis & Rheumatism

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Objective. To determine, in a case‐control study, if patients with new‐onset juvenile dermatomyositis (juvenile DM) have increased symptoms prior to onset, exposure to certain environmental conditions, frequency of familial autoimmune diseases, or antibody titers, compared with 2 control groups. Methods. A structured interview with the families of 80 children with juvenile DM, 40 children with juvenile rheumatoid arthritis (JRA), or 23 healthy children, from the same geographic area as the children with juvenile DM, was conducted. All children's sera were tested for antibody to Toxoplasma gondii, herpes simplex virus (HSV), or coxsackievirus B (CVB). Results. A high proportion of children with juvenile DM had constitutional symptoms 3 months before the disease‐onset date (P = 0.013 versus control children). Children with JRA had more relatives with rheumatoid arthritis (P = 0.0001) and pernicious anemia (P = 0.003) than did children with juvenile DM or healthy children. Among children ⩽7 years of age, elevated enteroviral titers were more frequent in those with juvenile DM (81%) and in healthy controls (90%) than in those with JRA (64%), suggesting a common environmental exposure. Titers to T gondii, HSV, or CVB 1‐6 were normal. Conclusion. Frequencies of familial autoimmune disease, exposure to environmental factors, or elevated antibody titers to T gondii, HSV, or CVB are not increased in juvenile DM. Children with juvenile DM do have symptoms of illness 3 months before the disease‐onset date, and young patients have elevated enteroviral titers, as do young geographic controls.

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Section: Discussionsupporting

confidence: 78%

Section: Demographic Characteristics Of the Study Groupsmentioning

confidence: 99%

New‐onset juvenile dermatomyositis. Comparisons with a healthy cohort and children with juvenile rheumatoid arthritis

Pachman

Hayford

Hochberg

et al. 1997

Arthritis & Rheumatism

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“…while coxsackie A9 has been reported in an adult with polymyositis (8). Travers et al (12) found fourfold or greater increases in neutralizing antibody to coxsackie B4 in 2 adults with dermatomyositis and 1 adult with polymyositis, and to coxsackie B3 in I adult with polymyositis. Their 2 dermatomyositis patients also exhibited heterotypic twofold increases in antibodies to B1 and B3.…”

Section: Discussionmentioning

confidence: 99%

Prevalence of Coxsackie B Virus Antibodies in Patients With Juvenile Dermatomyositis

Christensen

Pachman

Schneiderman

et al. 1986

Arthritis & Rheumatism

179

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A number of viruses have been implicated as being the cause of various forms of myositis, including acute transient myositis, chronic polymyositis, and dermatomyositis. However, the cause of juvenile dermatomyositis (JDM) has remained elusive. Our study of serum samples taken within 4 months of the onset of disease in 12 children with JDM showed that 83% had detectable titers of complement-fixing (CF) antibody to 1 or more coxsackie B viral antigens. Detectable titers were found in only 25% of age-, sex-, and date-matched control sera taken from 24 patients with juvenile rheumatoid arthritis (JRA), and in 25% of serum samples taken from 2,192 "normal" children who had been hospitalized because of viral syndromes. Titers of CF antibody to coxsackie B1, B2, and B4 were positive in 58%, SO%, and 58%, respectively, of the JDM patients.In matched JRA controls, the respective values were 8%, 13%, and 8%. There were no significant antiviral titers and no significant differences in the results of tests for 13 other viral CF antigens, hepatitis B surface antigen, and Mycoplasma pneumoniue CF antigen in the JDM patient sera compared with the JRA patient sera. When titers of neutralizing antibody were determined, 58%, 58%, and 67% of the JDM patients were positive for coxsackie B2, B4, and B5, respectively, whereas 16%, 26%, and 21%, respectively, of the JRA controls were positive for the 3 antigens. These data suggest that the host response to coxsackie B virus might be related to the pathophysiology of JDM.

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“…This association has arisen principally from retrospective serology (Christensen et al, 1986;Travers et al, 1977) as rarely can infectious virus be isolated or virus-specific antigens be detected by immunofluorescence in the affected tissue (Morgan-Capner et al, 1984). However, DNA hybridization studies have established that persisting enteroviral RNA can be detected in the affected tissue in a proportion of cases of patients with certain chronic muscle diseases (Bowles et al, 1986(Bowles et al, , 1987Archard et al, 1988).…”

mentioning

confidence: 99%

Persistence of enteroviral RNA in chronic fatigue syndrome is associated with the abnormal production of equal amounts of positive and negative strands of enteroviral RNA

Cunningham

Bowles

Lane

et al. 1990

Journal of General Virology

127

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A subgenomic restriction fragment from cDNA prepared from Coxsackie B2 virus (CVB2) RNA was snbcloned into a riboprobe vector allowing the production of enteroviral group-specific RNA probes complementary to either the positive (genomic) or negative (template) strand of enteroviral RNA. These riboprobes were used to follow productive infection of cultured cells by CVB2; as expected, positive strand RNA was synthesized in approximately 100-fold excess over negative strand. RNA was extracted from muscle biopsy samples from patients with chronic fatigue syndrome and probed for the presence of enteroviral RNA. In cases where enteroviral RNA was detected the amounts of positive and negative strands of enteroviral RNA were approximately equal, in contrast to the situation in tytic infection of cultured cells. This suggests that entrovirus pesistence in muscle is due to a defect in control of viral RNA synthesis.

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Coxsackie B Neutralisation Titres in Polymyositis/Dermatomyositis

Cited by 73 publications

References 10 publications

New‐onset juvenile dermatomyositis. Comparisons with a healthy cohort and children with juvenile rheumatoid arthritis

New‐onset juvenile dermatomyositis. Comparisons with a healthy cohort and children with juvenile rheumatoid arthritis

Prevalence of Coxsackie B Virus Antibodies in Patients With Juvenile Dermatomyositis

Persistence of enteroviral RNA in chronic fatigue syndrome is associated with the abnormal production of equal amounts of positive and negative strands of enteroviral RNA

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