Type Diabetes And Possible Association With Viral Infections

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Seasonal variation in the diagnosis of Type 1 diabetes has been considered as indirect evidence for environmental exposure in the development of Type 1 diabetes. Recent studies have provided more indirect evidence for an association between viral infections and the pathogenesis of insulin-dependent diabetes, but the final evidence for viruses causing insulin-dependent diabetes is still missing (114). Some communicable diseases occur more frequently during the cold winter months in areas where the climate changes during the year. Therefore infectious diseases could play a role, at least as a triggering factor in the onset of clinical symptoms of insulin-dependent diabetes.

Although a large number of common viruses, e.g. mumps, rubella and the Coxsackie B group, have been implicated as having a role in the development of Type 1 diabetes, this disease is not a common consequence of viral infection. Even though it was suggested in the last century that there might be a connection between mumps and Type 1 diabetes (115), the part that viruses play in Type 1 diabetes is still not clear. Many reports have shown a temporal relationship between certain viral infections and Type 1 diabetes, but whether viruses are directly responsible for damage to the pancreatic ^-cells in humans or whether they can cause diabetes by triggering an autoimmune response is unknown (116). In vitro, mumps virus, Coxsackie B3 and B4 virus, and reovirus type 3 can infect human pancreatic ^-cells and destroy them. In mice the encephalomyocar-ditis virus, the meningovirus and the Coxsackie B4 virus are able to destroy pancreatic ^-cells when inoculated, and in cattle a form of diabetes developed after an outbreak of foot-and-mouth disease (117). The number of well-documented case reports involving Coxsackie B viruses is small. However, they show that virus infections can trigger or be the final cause in the development of Type 1 diabetes, at least in some cases (118). An increased prevalence of Type 1 diabetes has been found in patients with congenital rubella (119-121) and it has been shown that rubella virus can multiply in the pancreas and cause lesions. Rubella used to be a very common cause of infection in many populations, but it has now been eradicated from many parts of world, e.g. from Northern Europe. However, at the same time an increasing trend in incidence does not support the potential role of rubella infection as a causal or triggering factor for onset of Type 1 diabetes.

Viruses are unlikely to be the major precipitating factors in Type 1 diabetes, otherwise the incidence of Type 1 diabetes should have fallen during the first decade of immunization against measles, rubella, mumps and poliomyelitis in the USA (122). In Finland, the country with the highest incidence of Type 1 diabetes in the world, the immunization programme against mumps and rubella was started in 1982. The incidence of Type 1 diabetes is still increasing in Finland (123), and the increase in incidence has been steepest among the youngest children since the mid-1980s.

Recent data from Sweden (124) and Finland (125) suggest that mothers whose children subsequently became diabetic had higher group-specific enterovirus antibodies during this particular pregnancy than mothers whose children remained non-diabetic. The mechanism of possible perinatal virus exposure remains unknown. A sequence similarity between Coxsackie B and glutamic acid decarboxylase (GAD) has been described (126), leading to speculations of possible molecular mimicry, but this hypothesis is unproven.

It must be borne in mind that many virus variants are grouped together under one name: for instance, the term 'Coxsackie virus B4' signifies at least 13 variants. It may be that only a rare variant of the Coxsackie virus B group is diabetogenic and that vaccination against this variant might be possible in the future.

It has been reported that diabetic patients had reduced titers of antibodies to reoviruses and reduced titers of IgG and IgM antibodies to mumps, compared with healthy controls, whereas mumps-specific IgA antibodies were found more frequently (128). These results suggest that the immunologic response to certain viruses is different in Type 1 diabetes patients compared with healthy people and may indicate that Type 1 diabetes patients have selective defects in their humoral response to certain viral antigens. This is clearly an area for further research with respect to prevention of Type 1 diabetes.

Although recent observations suggest that exposures to enterovirus infections both in utero and in childhood may be able to induce and promote fl-cell damage and thus lead to Type 1 diabetes, we do not have enough evidence to say that such infections are truly causing Type 1 diabetes. Many people hope that it will be possible to develop a vaccine to prevent Type 1 diabetes, but much more information is needed before it will be possible to provide sufficient evidence to justify such an approach. Vaccination may not simply remove a disease like Type 1 diabetes. Interestingly, it was noticed that the penetrance of diabetes in female NOD mice reared in a pathogen-free environment approaches 100% (126). After exposure to mouse hepatitis virus, only 35% of mice became diabetic.

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