Numerous studies have indicated that failure of the cellular immune response, including type 1 helper T cells (Th1) hypo-responsiveness, cytotoxic T lymphocyte (CTL) exhaustion, excessive function of CD4+  CD25+  FOXP3+ regulatory T cells, and failure of lymphoid cells via direct binding and/or infection in B cells, T cells, NK cells, and DCs occurs in CHC patients [9–21]. The gene discussed is CD4; the disease is infection.