Search

Type 1 diabetes is caused by pancreatic β-cell destruction that leads to loss of insulin secretion and absolute insulin deficiency. Type 1 diabetes accounts for about 10% of all diabetes, affecting approximately 1.4 million people in the U.S., and 10–20 million globally.1 Diabetes is one of the most common severe chronic diseases of childhood affecting 1 in 300 children and as many as 1 in 100 adults during the life span.2

Rubella infection especially during the first trimester of pregnancy can cause damages to the embryonic organs and may also result in late symptoms such as endocrinopathies and others. Prenatal diagnosis of fetal infection is difficult. IgM has been detected in fetal blood samples occasionally as early as 15 weeks of pregnancy. Unfortunately blood can be withdrawn under ultrasound guidance from the umbilical vein only after 20 weeks in many fetuses. Not every infection of pregnant women with Rubella virus causes prenatal damage of the child and so pregnancies were often interrupted unnecessarily. With the help of molecular biological methods we should be able to diagnose a prenatal Rubella infection earlier than in the 20th week of pregnancy.

Rubella virus infection of women during early stage of pregnancy often induces congenital defects in the newborn 1. Major defects include deafness, cataracts and heart disorders and are collectively known as Congenital Rubella Syndrome (CRS). At every epidemic of Rubella, there was reoccurence of babies born with CRS and also of a considerable number of artificial abortions because of the fear of having babies with CRS2.

Isolated deficiency of IgA is by far the most commonly identified defect of the immune system in humans. It occurs in individuals who are otherwise entirely healthy, but has also been frequently associated with such diverse disease states as congenital viral or parasitic infection, chromosomal abnormalities, and autoimmune diseases. Family studies have suggested that this condition may be inherited either as an autosomal dominant or recessive trait.

The efficacy of vaccination was illustrated in a dramatic way by the global eradication of smallpox ten years ago. Vaccination has also greatly reduced morbidity and mortality due to yellow fever in Africa and Central America. In the United States vaccination programs have nearly eliminated deaths from diphtheria, measles and mumps as well as paralytic poliomyelitis and the congenital rubella syndrome (Hilleman, 1985).

The frequency of Type I, or insulin-dependent mellitus (IDDM) in the general population is approximately 1 in 600 individuals. By contrast, in families where one child has IDDM, the likelihood that another child will develop IDDM is about 100 times higher. This population, at high risk for the development of IDDM, seemed an ideal group in which to identify some of the factors which might precede the development of clinically apparent IDDM. IDDM is clearly a multifactorial disease. The existence of a gene or genes predisposing to diabetes and mapping within or very near the HLA locus on chromosome six has been suggested by several different investigators. In addition, environmental agents also appear to be needed to “trigger” the predisposition towards overt disease since concordance for monozygotic twins is estimated at only approximately 30%. Convincing evidence has accumulated over the last several years that the mechanism of the expression of the genetic susceptibility is an autoimmune destruction of the pancreatic beta cells.

Three single-stranded RNA viruses cause childhood diseases for which vaccines are available. Measles and mumps are paramyxoviruses, and rubella is a togavirus. These viruses range in size from 50 to 270 nm and all have lipid coats with multiple surface projections containing a hemagglutinin and, in the case of mumps, a neuraminidase. They all undergo cytoplasmic replication with budding and are similarly “fragile” viruses. However, each is unique in its own way. These similarities and differences will be noted in this chapter, with a concentration on characteristics of host-virus interactions that explain human disease processes.

During the past 15 years ample evidence has been accumulated that immunological reactions are involved in the development of insulin-dependent diabetes mellitus, i.e. Type I diabetes. It is currently widely thought that insulin-deficiency results from a chronic, organ-specific autoimmune reaction ultimately resulting in beta-cell destruction. Despite abundant data on both humoral and cellular abnormal immunological patterns detectable during the clinically silent prediabetic period, to date unequivocal demonstration of a direct pernicious autoimmune lesion of the beta-cells is still missing (1). Based on epidemiological investigations, it is noted that environmental factors most likely trigger the disease process in susceptible individuals. In support of such an initiating event are the marked discordance rate of approximately 50% in identical twins (D. Pyke, Chapter 31), the increased frequency of children with Type I diabetes with the congenital rubella syndrome (2), and the enhancing and preventing effect of dietary constituents on the incidence of diabetes in the diabetes-prone BB rat (F.W. Scott, Chapter 34). In all these situations the participation of autoimmune signs is unquestionable, yet the beta-cell specific immunopathogenic pathway still remains to be defined.

Rubella was first recognized as a distinct disease entity in the early 1800’s (68). For the next 125 years, rubella virus was considered to cause only a mild morbilliform rash, occasional fever and a rather predictable lymphadenopathy. Predominantly a childhood disease, rubella is endemic throughout the world and is associated with epidemics which occur every six to nine years.