Tumor necrosis factor: The key to hepatitis B viral clearance

摘要

The immunopathogenesis of hepatitis B virus(HBV)involves a complex interaction of innate and adaptive immune response associated with several cytokines.However,due to experimental limitations,very limited and even no activation of the innate immune response can be demonstrated in acute HBV infection.The role of innate immunity and the key innate effectors for HBV clearance is still uncertain.It is also not clear whether clinical use of TNF inhibitors in treating rheumatoid arthritis and other autoimmune disease patients with chronic HBV infection would affect viral reactivation.However,in a recent paper in Cell Mol Immunol,Chyuan et al.reported that under TNF-αblockade,HBV viral clearance was impaired with persistent elevated HBV viral load in a dose and temporal-dependent manner.1 It demonstrates that a deficiency of TNF-αreduces viral clearance and promotes HBV persistence in a mouse model,and the impairment of HBV clearance under anti-TNF-αoccurs at an early time point of HBV infection,suggesting that HBV may reactivate during therapy with TNF inhibitors.The results together with previous reports support that TNF is a key innate cytokine required to clear HBV.2,3 It also provides evidence that therapy with TNF inhibitors may impair immune response to HBV clearance.