I’ve just been marking some student work about Group B coxsackieviruses as the cause of type 1 diabetes (T1D). This is a very old story, going back to the 1960s. In 1973 the discovery that Coxsackie virus B4 could induce insulin-dependent diabetes in suckling mice caused a lot of excitement, some of which is still bubbling away. The problem is that it is clear that Group B coxsackievirus infection in humans does not “cause” diabetes – in the sense of get infected, get diabetes. But the link won’t go away, so what is the connection between CVB and type 1 diabetes. A recent paper proposes a model which could explain the involvement of CVB as a contributory factor – if not the cause – of diabetes:
- Human β cells express enterovirus entry receptors and can sustain enterovirus replication.
- Acute infection of β cells can lead to extensive islet damage and to fulminant diabetes.
Persistent infection of β cells could drive islet autoimmunity and the development of T1D.
- The ‘strength’ of the β cell antiviral response may determine whether autoimmunity and T1D develop.
Enteroviruses as causative agents in type 1 diabetes: loose ends or lost cause? (2014) Trends in Endocrinology & Metabolism, 25(12), 611-619
Considerable evidence implies that an enteroviral infection may accelerate or precipitate type 1 diabetes (T1D) in some individuals. However, causality is not proven. We present and critically assess evidence suggesting that islet β cells can become infected with enterovirus, and argue that this may result in one of several consequences. Occasionally, a fully lytic infection may arise and this culminates in fulminant diabetes. Alternatively, an atypical persistent infection develops which can be either benign or promote islet autoimmunity. We propose a model in which the ‘strength’ of the β cell response to the establishment of a persistent enteroviral infection determines the final disease outcome.