Although the primary cause of type 2 diabetes is unknown, two breakthroughs have been made regarding its development (
1).
First, insulin resistance in muscle is the earliest detectable defect in people in whom type 2 diabetes will later develop.
Second, β-cell function has to be abnormal before hyperglycemia develops. One of the risk factors for diabetes development might be virus infection (
2)
CONCLUSIONS
A significant association of HSV-1 infection with type 2 diabetes was found in the present study. All subjects were hepatitis C virus antibody seronegative, so the confounding relationship between hepatitis C virus infection and type 2 diabetes can be excluded.
Chronic inflammation is involved closely and early on in the pathogenesis of type 2 diabetes (
10,
11). Viral infection of the pancreas, but not islets, can lead to induction of Fas on β-cells, which renders them susceptible to Fas/Fas-ligand-mediated apoptosis and resulting in a significant degree of clinically manifest diabetes (
12). HSV-1 DNA might reside in surviving HSV-1-infected mice in a “latent” state in pancreas (
13). HSV-1 infection can cause the pancreas multiple small foci of hemorrhagic necrosis in humans (
14) and could induce the production of cytokines and inflammation response (
15,
16).