We assume that strong immune pressure derived from passive-active immunization against HBV could allow the establishment of a low-dose HBV infection without sufficient antigens to stimulate and maintain the maturation of immune memory, which was supported by discoveries in woodchuck infection model that exposure to low levels of HBV DNA (<103 virions) might develop into anti-HBc seronegative infection [19]. The gene discussed is KRT88P; the disease is infection.