CONCLUSION : The polymorphisms of proinflammatory cytokines are related to the serum lipoprotein level in these subjects.
Cytokine genes are polymorphic at specific sites , and certain mutations located within coding/regulatory regions have been shown to affect the overall expression and secretion of cytokines.
Herein , we illustrate that virus-specific CD4 T cells are functionally inactivated early during the transition into viral persistence and fail to produce effector cytokines (i.e. , interleukin-2 and tumor necrosis factor alpha) , thereby compromising an efficient and effective antiviral immune response.
Thus , viruses subvert the known antiviral effect of type I IFN through STAT2-specific signaling to benefit their survival.