Autoimmunity and viral infection in diabetes mellitus.
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Forty-three newly diagnosed insulin-dependent diabetics and thirty control subjects have been examined for cellular hypersensitivity to different pancreatic preparations, rat liver mitochondria and Coxsackie B4 virus. Evidence for cellular hypersensitivity to the pancreatic preparations was shown in the diabetic group, in whom the hypersensitivity to the pancreatic preparations was found to correlate with hypersensitivity to rat liver mitochondria. Hypersensitivity to Coxsackie B4 virus was not found to differ significantly in the diabetic and control groups. Hypersensitivity to liver mitochondria appeared to decrease over a 1-year period. There was an indication that hypersensitivity to Coxsackie B4 was greatest 3 months after diagnosis. (+info)
Maturation of intestinal defenses against peroral infection with group B coxsackievirus in mice.
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The intestinal tract of adult mice provides effective protection against peroral infection with group B coxsackievirus. This protective function consists of at least two separate components. One is a barrier effect that prevents virus from passing through the mucosal side of the gut into the circulation. It becomes clearly evident at 18 days of life and is present thereafter. The other is a clearance mechanism that acts to eliminate virus from the enteric tract after infection has occurred. This is first demonstrable at about 14 to 18 days and also persists. The appearance of these protective functions coincides with the known development of enzymatic and morphological changes in the gut associated with the transition from suckling to weanling. (+info)
beta2-microglobulin-associated regulation of interferon-gamma and virus-specific immunoglobulin G confer resistance against the development of chronic coxsackievirus myocarditis.
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To gain insight into the strategies of the immune system to confer resistance against the development of chronic coxsackievirus B3 (CVB3) myocarditis we compared the course of the disease in C57BL/6 mice, beta2-microglobulin knockout (beta2m(-/-)) mice, and perforin-deficient (perforin(-/-)) mice. We found that perforin(-/-) mice as well as immunocompetent C57BL/6 mice reveal a resistant phenotype with complete elimination of the virus from the heart in the course of acute myocarditis. In contrast, myocardial CVB3 infection of beta2m(-/-) mice was characterized by a significantly higher virus load associated with a fulminant acute inflammatory response and, as a consequence of virus persistence, by the development of chronic myocarditis. Interferon-gamma secretion of stimulated spleen cells was found to be significantly delayed in beta2m(-/-) mice compared to perforin(-/-) mice and C57BL/6 control mice during acute myocarditis. In addition, generation of virus-specific IgG and neutralizing antibodies were found to be significantly decreased in beta2m(-/-) mice during acute infection. From these results we conclude that protection against the development of chronic myocarditis strongly depends on the expression of beta2m, influencing the catabolism of IgG as well as the production of protective cytokines, such as interferon-gamma. Moreover, CVB3-induced cardiac injury and prevention of chronic myocarditis was found to be unrelated to perforin-mediated cytotoxicity in our model system. (+info)
Successful treatment of enterovirus-infected mice by 2-(alpha-hydroxybenzyl)-benzimidazole and guanidine.
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Echo virus 9- or Coxsackie A 9-infected newborn mice are protected from paralysis and death by combined treatment with nontoxic concentrations of HBB plus guanidine. HBB alone also protects Coxsackie A 9, but not echo virus 9-infected animals, whereas guanidine alone is ineffective in either case. Protection is due to inhibition of virus multiplication via the antiviral activity of these selective inhibitors. Treatment must be begun at the latest 48 h after virus inoculation. 3 days of treatment are sufficient if started at the time of virus inoculation. Failure of protection after treatment with one compound alone is not due to rapid development of drug-resistant virus mutants. Infected, successfully treated mice may develop a solid immunity. (+info)
Selenium deficiency and viral infection.
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The discovery that the juvenile cardiomyopathy known as Keshan disease likely has a dual etiology that involves both a nutritional deficiency of the essential trace mineral selenium (Se) as well as an infection with an enterovirus provided the impetus for additional studies of relationships between nutrition and viral infection. An amyocarditic strain of coxsackievirus B3, CVB3/0, converted to virulence when it was inoculated into Se-deficient mice. This conversion was accompanied by changes in the genetic structure of the virus so that its genome closely resembled that of other known virulent CVB3 strains. Similar alterations in virulence and genomic composition of CVB3/0 could be observed in mice fed normal diets but genetically deprived of the antioxidant selenoenzyme glutathione peroxidase (knockout mice). More recent research has shown that a mild strain of influenza virus, influenza A/Bangkok/1/79, also exhibits increased virulence when given to Se-deficient mice. This increased virulence is accompanied by multiple changes in the viral genome in a segment previously thought to be relatively stable. Epidemic neuropathy in Cuba has features that suggest a combined nutritional/viral etiology. Further research, both basic and applied, is needed to assess properly the possible role of malnutrition in contributing to the emergence of novel viral diseases. (+info)
Heart disease caused by Coxsackie virus B infection.
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A study of 55 patients with heart disease suspected of being viral in origin was carried out a Medical College Hospital, Nagpur, over a period of 2 years. Virus studies as well as other routine tests were carried out on all patients. In 19 patients a virus aetiology of the heart disease was proved by isolation of one of the subtypes of Coxsackie B virus and/or on the basis of fourfold rise in neutralizing antibody titre in paired sera. Of these patients, 5 had acute myocarditis and 5 had acute myopericarditis; 3 had acute pericarditis; 3 had congestive cardiac failure of obscure aetiology; 2 had pleuropericarditis, and the remaining 1 developed post-partum heart failure with cardiogenic shock. All had electrocardiographic abnormalities. Thirteen had cardiomegaly; 1 had a right-sided pleural effusion and 2 had pericardial effusion. Virus could not be isolated from pericardial fluid or pleural fluid in these 3 patients. Follow-up studies up to 10 weeks from discharge revealed that 8 patients were clinically normal but 4 of these 8 had persisting ST-T wave changes, and in 4 the electrocardiogram had returned to normal. Of the remaining 11 patients, 3 had persistent chronic heart failure, 3 had vague symptoms of praecordial pain but no abnormal signs, and 5 patients were lost to follow-up. (+info)
Severe rhabdomyolysis and acute renal failure following recent Coxsackie B virus infection.
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Viral infections have been associated with a wide spectrum of muscle disorders, ranging from acute nonspecific myalgia to myositis. However, severe rhabdomyolysis, with or without accompanying acute renal failure (ARF), has been described only rarely. We report the fourth case in the literature of recent Coxsackie B virus infection complicated by severe rhabdomyolysis and ARF, necessitating temporary haemodialysis in a previously healthy young man. Although most Coxsackie B virus infections are asymptomatic, one should be aware of this potentially life-threatening complication of this virus. As illustrated with the present case, serological testing may reveal the diagnosis in a case of rhabdomyolysis after a viral illness. (+info)
Heparan sulfates and coxsackievirus-adenovirus receptor: each one mediates coxsackievirus B3 PD infection.
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Amino acid exchanges in the virus capsid protein VP1 allow the coxsackievirus B3 variant PD (CVB3 PD) to replicate in decay accelerating factor (DAF)-negative and coxsackievirus-adenovirus receptor (CAR)-negative cells. This suggests that molecules other than DAF and CAR are involved in attachment of this CVB3 variant to cell surfaces. The observation that productive infection associated with cytopathic effect occurred in Chinese hamster ovary (CHO-K1) cells, whereas heparinase-treated CHO-K1 cells, glucosaminoglycan-negative pgsA-745, heparan sulfate (HS)-negative pgsD-677, and pgsE-606 cells with significantly reduced N-sulfate expression resist CVB3 PD infection, indicates a critical role of highly sulfated HS. 2-O-sulfate-lacking pgsF-17 cells represented the cell line with minimum HS modifications susceptible for CVB3 PD. Inhibition of virus replication in CHO-K1 cells by polycationic compounds, pentosan polysulfate, lung heparin, and several intestinal but not kidney HS supported the hypothesis that CVB3 PD uses specific modified HS for entry. In addition, recombinant human hepatocyte growth factor blocked CVB3 PD infection. However, CAR also mediates CVB3 PD infection, because this CVB3 variant replicates in HS-lacking but CAR-bearing Raji cells, infection could be prevented by pretreatment of cells with CAR antibody, and HS-negative pgsD-677 cells transfected with CAR became susceptible for CVB3 PD. These results demonstrate that the amino acid substitutions in the viral capsid protein VP1 enable CVB3 PD to use specific modified HS as an entry receptor in addition to CAR. (+info)