Fig. 2.

Pro-diabetic effects of viral infection. Viral infection activates a Type-I immune response, resulting in the production of cytokines such as TNF, IFNγ and IL-6. These induce transient insulin resistance in muscle and liver. The pancreas compensates IR through increased secretion of insulin, which directly promotes the antiviral immune system. In obesity, cytokine-induced IR can contribute to the formation of IR. In addition, several viruses infect the pancreas, which negatively impacts its ability to produce insulin. This may also contribute to loss of pancreatic β-cell function.