A study of Coxsackie B virus infections, 1972–1983

Bell, Eleanor J.; McCartney, R.A.

doi:10.1017/s0022172400064718

Cited by 39 publications

(10 citation statements)

References 9 publications

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“…Many viruses, notably the enteroviruses, have been implicated in the aetiology of CFS [23]. Neutralizing antibody to Coxsackie B virus (CBV) is commonly found in the blood [24][25][26][27]. Coxsackie virus-specific RNA has been reported in skeletal muscle biopsies [28,29].…”

Section: Virusesmentioning

confidence: 99%

Chronic fatigue syndrome—aetiological aspects

Dickinson

1997

Eur J Clin Investigation

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The chronic fatigue syndrome (CFS) has been intensively studied over the last 40 years, but no conclusions have yet been agreed as to its cause. Most cases nowadays are sporadic. In the established chronic condition there are no consistently abnormal physical signs or abnormalities on laboratory investigation. Many physicians remain convinced that the symptoms are psychological rather than physical in origin. This view is reinforced by the emotional way in which many patients present themselves. The overlap of symptoms between CFS and depression remains a source of confusion and difficulty. But even if all CFS patients were rediagnosed as depressives, this would not negate the possibility of an underlying organic cause for the condition, in view of the growing evidence that depression itself has a physical cause and responds best to physical treatments. There is some evidence both for active viral infection and for an immunological disorder in the CFS. Many observations suggest that the syndrome could derive from residual damage to the reticular activating system (RAS) of the upper brain stem and/or to its cortical projections. Such damage could be produced by a previous viral infection, leaving functional defects unaccompanied by any gross histological changes. In animal experiments activation of the RAS can change sleep state and activate or stimulate cortical functions. RAS lesions can produce somnolence and apathy. Studies by modern imaging techniques have not been entirely consistent, but many magnetic resonance imaging (MRI) studies already suggest that small discrete patchy brain stem and subcortical lesions can often be seen in CFS. Regional blood flow studies by single photon-emission computerized tomography (SPECT) have been more consistent. They have revealed blood flow reductions in many regions, especially in the hind brain. Similar lesions have been reported after poliomyelitis and in multiple sclerosis--in both of which conditions chronic fatigue is characteristically present. In the well-known post-polio fatigue syndrome, lesions predominate in the RAS of the brain stem. If similar underlying lesions in the RAS can eventually be identified in CFS, the therapeutic target for CFS would be better defined than it is at present. A number of logical approaches to treatment can already be envisaged.

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Section: Virusesmentioning

confidence: 99%

Chronic fatigue syndrome—aetiological aspects

Dickinson

1997

Eur J Clin Investigation

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“…It is possible that both a particular genetic make-up of the host and the appropriate strain are necessary for diabetogenesis, as proposed by Roivainen et al [7]. In addition, studies in the past have revealed that, at least for some individuals, infection with a different Coxsackievirus B serotype can increase the levels of antibody against a previously infecting serotype (heterotypic response) [8]. The lack of uniformity of presence of antibodies against all serotypes at old ages argues against heterotypic antibody responses being common.…”

Section: Discussionmentioning

confidence: 99%

The association between prior infection with five serotypes of Coxsackievirus B and incident type 2 diabetes mellitus in the EPIC-Norfolk study

et al. 2012

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Aims/hypothesis Infections with Coxsackieviruses have been linked to beta cell dysfunction. Given the importance of beta cell dysfunction in the aetiology of type 2 diabetes, we hypothesised that prior infection with Coxsackieviruses B would increase the risk of type 2 diabetes. The aims of the study were to estimate cross-sectional associations between potential predictors of previous infection and seropositivity for Coxsackievirus B serotypes 1-5 (CBV1-5), and then to assess the association between seropositivity and incident type 2 diabetes.Methods Using a case-cohort design nested within the European Prospective Investigation of Cancer (EPIC)-Norfolk study, we ascertained n0603 cases of incident type 2 diabetes. From within the entire cohort we identified a random subcohort of n0835, without diabetes at baseline. The presence of Coxsackievirus B neutralising antibodies against serotypes 1-5 was assessed using a plaque neutralisation assay. Weighted Cox regression was used to examine the association between presence of antibodies to CBV1-5 and the development of type 2 diabetes. Results Seropositivity in the subcohort for CBV1-5 was 50%, 67%, 66%, 75% and 45%, respectively. After adjustment for age, sex, BMI, physical activity and family history of diabetes, the presence of antibodies against CBV1-5 was not associated with incident type 2 diabetes, over a mean follow-up of 5.

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“…Coxsackieviruses have the potential to cause a wide variety of symptoms in a normally healthy host. These include high fever, vomiting, abdominal pain, headache, rash, jaundice, and diarrhea, and serious health outcomes such as aseptic meningitis (Bell & McCartney, 1984), myocarditis (Bowles et al, 1986; Reyes & Lerner, 1985; Bell & McCartney, 1984; Kaplan et al, 1983; Artenstein et al, 1965), respiratory illness (Bloom et al, 1962), encephalitis (Bowles et al, 1986; Reyes & Lerner, 1985; Moore et al, 1984; Kaplan et al, 1983; Artenstein et al, 1965; Bloom et al, 1962), and insulin‐dependent diabetes mellitus (IDDM) (Frisk et al, 1992; Sumbureru, 1991; Yoon, 1990; Barrett‐Connor, 1985; Bell & McCartney, 1984). Because of this range of symptoms and outcomes, outbreaks as well as the importance of coxsackievirus infections may go unrecognized.…”

Section: Coxsackievirus Backgroundmentioning

confidence: 99%

Risk Assessment of waterborne coxsackievirus

Mena¹,

Gerba²,

Haas³

et al. 2003

Journal AWWA

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Virus contamination of the water environment through disposal of human wastewater remains a concern for the water industry. Coxsackieviruses are the most common nonpolio enteroviruses found in domestic wastewater and in contaminated surface water, groundwater, and drinking water. Although most infections result in mild febrile illness, coxsackieviruses are capable of causing a wide range of serious illnesses (including aseptic meningitis, myocarditis, and respiratory illness) and are associated with cases of insulin‐dependent diabetes mellitus. A risk assessment approach was used to evaluate the potential public health effects associated with contaminated drinking water and recreational waters. An exponential model developed from human dose–response studies was used to describe the infectivity of coxsackievirus type B and estimate daily and yearly risks of infection, morbidity, and mortality. Concentrations of coxsackievirus reported in the literature were used to examine potential exposure. Although risks of infection for coxsackievirus are lower than for rotavirus, levels detected during outbreaks resulted in risks of 10–1 annually for drinking water. Risks assuming an ingestion of 100 mL per swim were 10–2 for a 10‐day exposure to freshwater. The severity of the diseases associated with this type of virus and its widespread contamination emphasize the importance of maintaining reliable wastewater and drinking water treatment.

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A study of Coxsackie B virus infections, 1972–1983

Cited by 39 publications

References 9 publications

Chronic fatigue syndrome—aetiological aspects

Chronic fatigue syndrome—aetiological aspects

The association between prior infection with five serotypes of Coxsackievirus B and incident type 2 diabetes mellitus in the EPIC-Norfolk study

Risk Assessment of waterborne coxsackievirus

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