Common Group of Viruses Strongly Linked to Type 1 Diabetes

Individuals with type 1 diabetes are eight times more likely than others to have an enterovirus infection; the findings support ongoing research on vaccines to help prevent the development of type 1 diabetes.

A new study recently presented at the annual conference of the European Association for the Study of Diabetes in Stockholm, Sweden, reveals a high association between a common group of viruses and type 1 diabetes (T1D).

According to the Australian study, those with T1D had an eight-fold higher risk of contracting an enterovirus infection than people without the condition.

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T1D is the most prevalent form of diabetes in children, and its prevalence has been rising globally in recent decades. The immune system attacks and destroys the insulin-producing beta cells in the pancreas of patients with the disease, preventing the body from making enough of the hormone to properly regulate blood sugar levels.

High blood sugar levels may reduce life expectancy and damage the kidneys, feet, eyes, heart, and eyes over time. Additionally, diabetic ketoacidosis, a disease that often occurs at the time of T1D diagnosis and involves the accumulation of dangerous substances known as ketones in the blood, may be fatal if not treated promptly.

Although the specific cause of the immune system’s response is still up for debate, it is generally accepted that a genetic predisposition and one or more environmental triggers, such as a viral infection, are involved.

Some of the strongest evidence for virus involvement points toward the enteroviruses. This very common group of viruses includes those that cause polio and hand, foot, and mouth disease (HFMD), as well as other types that cause milder, cold-like symptoms.

Vaccines that seek to reduce the incidence of T1D by preventing enterovirus infection are already in clinical trials1 and confirmation of the role of enteroviruses would support this and other work toward the primary prevention of T1D.

To explore the association more deeply, Sonia Isaacs, of the Department of Paediatrics and Child Health, School of Clinical Medicine, University of New South Wales, Australia, and colleagues carried out a systematic review and meta-analysis of existing research on the topic.

The meta-analysis – the largest in this field – included data on 12,077 participants (age 0-87 years) from 60 controlled observational studies found on the PubMed and Embase databases.

5,981 of the participants had T1D or islet autoimmunity (which typically progresses to T1D). The remaining 6,096 participants had neither condition.

Enterovirus RNA or protein, a sign of a current or recent infection, was detected in blood, stool, or tissue samples using a range of advanced, and highly sensitive, molecular techniques.

Those with islet autoimmunity had twice the odds of testing positive for enteroviruses as those without islet autoimmunity.

The odds of enterovirus infection were eight times greater in those with T1D than in those without T1D.

Most importantly, individuals with T1D were over 16 times more likely to have an enterovirus infection detected in the month after their T1D diagnosis than those without T1D.

The researchers conclude that there is a clear association between enterovirus infection and both islet autoimmunity and T1D.

Ms. Isaacs adds: “These findings provide further support for ongoing work to develop vaccines to prevent the development of islet autoimmunity and therefore reduce the incidence of T1D.”

There are several theories about how enteroviruses increase the risk of developing T1D. It is thought, for example, that their interaction with particular genes may be important.

Ms. Isaacs explains: “Our study found that people with T1D who had both genetic risk and a first-degree relative with T1D were 29 times more likely to have an enterovirus infection.”

She continues, “The number, timing and duration, and even the site of enterovirus infections may also be important. The ‘leaky gut’ hypothesis suggests that viruses originating in the gut could travel along with activated immune cells to the pancreas, where a low-level, persistent infection and resulting inflammation can lead to an autoimmune response. Virus infections are also proposed to work in combination with other factors such as diet, imbalances in the gut microbiome, and even chemical exposures which may occur in utero (during pregnancy) or early childhood. There is still a lot to learn.”

Reference: This press release is based on abstract 236 at the annual meeting of the European Association for the Study of Diabetes (EASD). The material has been peer reviewed by the congress selection committee. The research will soon be submitted to a medical journal but the full paper is not yet available.