The group of common viruses closely related to ty

A common group of viruses is closely related to type 1 diabetes (T1D), according to new research being presented at the annual meeting of the European Society for the Study of Diabetes in Stockholm, Sweden (September 19-23).

The Australian analysis found that individuals with T1D were eight times more likely to develop enterovirus infection than those without T1D.

T1D is the most common form of childhood diabetes and its incidence has been increasing worldwide in recent decades. In people with this condition, the immune system attacks and destroys insulin-producing beta cells in the pancreas, preventing the body from producing enough of the hormone to properly regulate blood sugar levels.

Over time, high blood sugar levels can damage the heart, eyes, feet, and kidneys and can shorten life expectancy. In addition, diabetic ketoacidosis, a condition often seen when T1D is diagnosed and involves the buildup of harmful substances called ketones in the blood, can be life-threatening if not treated early.

The cause of the immune system attack is still controversial, but it is believed to involve a combination of genetic predisposition and one or more environmental triggers such as a viral infection.

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

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

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

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

5,981 of the participants had T1D or islet autoimmunity (which usually progresses to T1D). The remaining 6,096 participants did not have any condition.

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

Those with islet autoimmunity are twice as likely to be tested for enteroviruses as those without islet autoimmunity.

The odds of contracting enterovirus were eight times higher in those with T1D than in those without T1D.

Importantly, individuals with T1D were 16 times more likely to have an enterovirus infection detected in the month following T1D diagnosis, than those without T1D.

The authors 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 the ongoing work of vaccine development to prevent the development of islet autoimmunity and thus 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 certain genes may be important.

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

The number, timing, duration, and even location of enterovirus infections may also be important. The ‘leaky gut’ hypothesis suggests that viruses originating in the gut can travel with activated immune cells to the pancreas, where low-level, persistent infection and the resulting inflammation can trigger an autoimmune response.

“It is also suggested that viral infection works in conjunction with other factors such as diet, imbalances in the gut microbiome and even exposure to chemicals that may occur in utero (during pregnancy) or early childhood. There is still much to learn.”

Ms. Sonia Isaacs, Department of Pediatrics and Child Health, School of Clinical Medicine, University of New South Wales School of Medicine, Australia. Tel: +61452500425 e)

annalisa.giosue@gmail.comAlternate contact: Tony Kirby at EASD Media Center. Tel) +44 7834 385827 H)

Notes to editors:



The authors have no conflict of interest to declare.

This press release is based on Abstract 236 of the European Association for the Study of Diabetes (EASD) annual meeting. The materials were reviewed by the conference’s peer selection committee. The research will soon be submitted to a medical journal but the full paper is not yet available.

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