For example, diabetes, hyperglycemia, and insulinogenic attenuate the synthesis of pro-inflammatory cytokines, such as IFN-γ and interleukins, to functionally impair the innate and humoral immune systems of the host.[41] Furthermore, cytokine overload related to the Th1 to Th2 shift in severe viral infection, when accompanied by increased cytokine synthesis from metabolic diseases, can be detrimental in synergistically affecting the endothelium and leads to a range. The gene discussed is IFNG; the disease is metabolic disease.