A genetically determined host factor controlling susceptibility to encephalomyocarditis virus-induced diabetes in mice

Kang, Yup; Yoon, Ji‐Won

doi:10.1099/0022-1317-74-6-1207

Cited by 29 publications

(24 citation statements)

References 28 publications

(43 reference statements)

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“…The data are consistent with the idea that EMC virus-induced diabetes follows Mendelian inheritance and that susceptibility is controlled by a single locus [78]. More recent experiments, in combination with earlier data, have indicated that a single gene controlling susceptibility to EMC-D virus-induced diabetes in mice can operate by modulating the expression of viral receptors on the beta cells [79].…”

Section: Control Of Emc Virus-induced Diabetes In Mice By the Viral Asupporting

confidence: 87%

The role of viruses in Type I diabetes: two distinct cellular and molecular pathogenic mechanisms of virus-induced diabetes in animals

2001

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Type I (insulin-dependent) diabetes mellitus results from the progressive destruction of insulin-producing pancreatic beta cells, which leads to the development of hypoinsulinaemia and hyperglycaemia [1±8]. It is believed that genetic factors are a major component in the aetiology of Type I diabetes because a strong association has been observed between susceptibility to Type I diabetes and specific alleles of the MHC class II genes [9±17]. Although genetic susceptibility seems to be a prerequisite, studies on the risk of developing Type I diabetes using genetically identical twins have shown that their concordance rate for the Diabetologia (2001)

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Section: Control Of Emc Virus-induced Diabetes In Mice By the Viral Asupporting

confidence: 87%

The role of viruses in Type I diabetes: two distinct cellular and molecular pathogenic mechanisms of virus-induced diabetes in animals

2001

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“…Infection of genetically susceptible mice with the M variant of EMC virus resulted in the selective destruction of pancreatic beta cells [132] (Figure 4). Further research found that beta cell destruction in EMC virus-infected mice is dependent on the genetic makeup of the virus and the genetic background of the host [133][134][135][136][137][138][139][140].…”

Section: Encephalomyocarditis Virusmentioning

confidence: 99%

A New Look at Viruses in Type 1 Diabetes

Jun¹,

Yoon²

2004

ILAR Journal

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Type 1 diabetes results from the destruction of pancreatic beta cells. Genetic factors are believed to be a major component for the development of type 1diabetes, but the concordance rate for the development of diabetes in identical twins is only about 40%, suggesting that non-genetic factors play an important role in the expression of the disease. Viruses are one environmental factor that is implicated in the pathogenesis of type 1 diabetes. To date, 14 different viruses have been reported to be associated with the development of type 1 diabetes in humans and animal models. Viruses may be involved in the pathogenesis of type 1 diabetes in at least two distinct ways: by inducing beta cellspecific autoimmunity, with or without infection of the beta cells, (e.g. Kilham rat virus) and by cytolytic infection and destruction of the beta cells (e.g. encephalomyocarditis virus in mice). With respect to virus-mediated autoimmunity, retrovirus, reovirus, Kilham rat virus, bovine viral diarrhoea-mucosal disease virus, mumps virus, rubella virus, cytomegalovirus and Epstein-Barr virus are discussed. With respect to the destruction of beta cells by cytolytic infection, encephalomyocarditis virus, mengovirus and Coxsackie B viruses are discussed. In addition, a review of transgenic animal models for virus-induced autoimmune diabetes is included, particularly with regard to lymphocytic choriomeningitis virus, influenza viral proteins and the EpsteinBarr viral receptor. Finally, the prevention of autoimmune diabetes by infection of viruses such as lymphocytic choriomeningitis virus is discussed.

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“…As with other picornaviruses, it consists of 4 capsid proteins, 3 of which (VP1, VP2, and VP3) are exposed on the surface of the virion. Among the 3, VP1, the major outer capsid protein, is believed to play an important role for virus attachment and immunogenicity (31,32).…”

Section: Discussionmentioning

confidence: 99%

Prevention of encephalomyocarditis virus-induced diabetes by live recombinant Mycobacterium bovis bacillus Calmette-Guérin in susceptible mice.

et al. 2000

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Recently, several live recombinant vaccine vehicles are being developed to produce a new generation of vaccines against a broad spectrum of infectious diseases. Among the possible bacterial and viral vaccine vector candidates, Mycobacterium bovis bacillus Calmette-Guérin (BCG) is particularly attractive because of specific characteristics such as low toxicity, adjuvant potential (14), low cost, and long-lasting immunity-inducing capacity (15,16). Recombinant BCG (rBCG) expressing foreign antigens is a promising candidate for the development of future vaccines and has been shown in several experimental models to induce protective immunity against viral, bacterial, or parasitic infections. Stover et al. (17) developed shuttle plasmids that are capable of autonomous replication in Escherichia coli and BCG. Since then, many investigators have constructed rBCG as a vaccine candidate against multiple pathogens and have examined its use as a live vaccine (17)(18)(19)(20)(21)(22)(23).This work was initiated to see whether the rBCG system is applicable for the prevention of virus-induced diabetes in the animal model. We have cloned the VP1 gene of the EMC virus into a BCG expression plasmid and transformed it into BCG. SJL/J male mice were immunized with rBCG and then were challenged with the highly diabetogenic EMC-D virus. None of the rBCG-immunized mice became diabetic, whereas control or vector-transformed BCG-immunized mice developed diabetes during the same challenge. The rBCGs were found to express VP1 efficiently in vitro and could induce substantial amounts of neutralizing antibodies and delayed-type hypersensitivity (DTH) to the EMC virus in the immunized animals. The rBCG-induced preventive immunities lasted longer than 10 months in the immunized mice. These long-lasting immunities are likely to be associated more with VP1-specific cellular immunity than with humoral immunity.

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A genetically determined host factor controlling susceptibility to encephalomyocarditis virus-induced diabetes in mice

Cited by 29 publications

References 28 publications

The role of viruses in Type I diabetes: two distinct cellular and molecular pathogenic mechanisms of virus-induced diabetes in animals

The role of viruses in Type I diabetes: two distinct cellular and molecular pathogenic mechanisms of virus-induced diabetes in animals

A New Look at Viruses in Type 1 Diabetes

Prevention of encephalomyocarditis virus-induced diabetes by live recombinant Mycobacterium bovis bacillus Calmette-Guérin in susceptible mice.

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