It is well documented that an appropriate adaptive immune response is required to efficiently control the HBV infection. T cell-mediated immune response directed against 2 Hepatitis Research and Treatment hepatitis B virus antigens is crucial for resolution of the infection [8] [9] [10] [11] [12] . HBV-specific CD8 + T cells are able to clear HBV-infected hepatocytes by secretion of Th1 antiviral cytokines, such as interferons (IFNs) and tumor necrosis factor alpha (TNFα), and direct cytotoxic mechanisms (perforin/granzyme, ligand-ligand induced cell death, e.g., Fas-Fas-L) [12] [13] [14] [15] [16] . An early, vigorous, polyclonal, and multispecific cellular immune response against the viral proteins is associated with the clearance of hepatitis B in acutely-infected patients. In contrast, chronic HBV carriers demonstrate weak, transient, or often undetectable CD8 + T cell response that correlates with HBV persistence [17] [18] [19] [20] [21] . Humoral immune response, especially neutralizing antienvelope antibodies, play a key role in preventing HBV spread to noninfected hepatocytes [20, 22] .