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Curr Diab Rep. 2019 Nov 21;19(12):141. doi: 10.1007/s11892-019-1256-9.

Human Endogenous Retroviruses and Type 1 Diabetes.

Author information

1
GeNeuro Innovation, 60 avenue Rockefeller, 69008, Lyon, France. sl@geneuro.com.
2
GeNeuro Innovation, 60 avenue Rockefeller, 69008, Lyon, France.
3
Faculté de Médecine, CHU Lille, Laboratoire de Virologie EA3610, Université Lille, F-59000, Lille, France.
4
Laboratoire des déficits immunitaires, University of Lyon, Lyon, France.
5
Plan-les-Ouates, GeNeuro SA, Geneva, Switzerland.

Abstract

PURPOSE OF THE REVIEW:

The aim of this review is to discuss recent data pointing at an involvement of human endogenous retroviruses (HERVs) in type 1 diabetes (T1D) onset and progression.

RECENT FINDINGS:

The envelope protein of HERV-W family, named HERV-W-Env, was detected in pancreata from T1D patients and was shown to display pro-inflammatory properties and direct toxicity toward pancreatic beta cells. The etiopathogenesis of T1D remains elusive, even if conventional environmental viral infections have been recurrently involved. Nonetheless, a new category of pathogens may provide the missing link between genetic susceptibility and environmental factors long thought to contribute to T1D onset. A number of studies have now shown that HERV sequences, which are normally inactivated or repressed in the human genome, could be activated by environmental viruses. Thus, if similarly activated by viruses associated with T1D, disregarded HERV genes may underlie T1D genetic susceptibility. Moreover, once expressed, HERV elements may display broad pathogenic properties, which identify them as potential new therapeutic targets.

KEYWORDS:

Coxsackievirus B4; Endogenous retrovirus; Enterovirus; HERV; Type 1 diabetes

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