Hepatitis B virus acquisition and pathogenesis in childhood: host genetic determinants

The clinical course of hepatitis B virus (HBV) infection varies from spontaneous recovery to chronic persistent infection leading to severe liver injury. Mounting evidence has recently highlighted the influence of host genotype in the complex interplay between viral and host factors. Studies in adults have suggested the existence of a genetic predisposition to HBV infection secondary to certain defects in the host response. These defects include opsonic deficiency, compromised antigen processing and presentation by human leucocyte antigen variations, attenuated T- and B-cell response, impaired cytokine and chemokine release, and production of receptors for several pertinent factors such as vitamin D and estrogen. By contrast, little is known about the genetic factors involved in the susceptibility to HBV transmission in early childhood. Herein, we review the literature regarding the association between host genetics and susceptibility to primary HBV infection, and we discuss the prospects of investigation in this field. A better understanding of HBV infection immunopathogenesis in the critical period of infancy may allow the development of optimal and innovative prevention and treatment.