Hepatitis B Virus Acquisition and Pathogenesis in Childhood: Host Genetic Determinants

Abstract

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.

Distribution OfCCR-5Δ32,CCR2-64I, andSDF-1-3′AAlleles Among Jordanians

“…This has been attributed to differences between individuals regarding genetic background and/or environmental factors such as diet and life style. [1][2][3] Genetic variations in certain chemokines and their receptors have been reported to be responsible for resistance to HIV-1 infection, delayed progression to AIDS, response to the treatment, and mother-to-child transmission. 4 Chemokine receptors are proteins found on the cell surface.…”

The ROLE OF GENETIC POLYMORPHISMS OF GENE IL-1β (-31 Т/С) AND IL-6 (-174 G/C) IN THE COURSE OF CHRONIC HEPATITIS B AND C IN CHILDREN

“…В патогенезе вирусных гепатитов у детей выделена роль таких факторов, как сниженный иммунный ответ Т-и В-клеток, нарушение продукции цитокинов, изменения гормональной регуляции [8]. Вместе с тем исследования влияния генетических факторов на клиническое течение болезни изучены преимущественно у взрослых пациентов.…”

Neonatal Cholestasis

“…However, in certain parts of the world, where universal HBV vaccinations are not effective, perinatal transmission of HBV occurs from a chronic carrier mother or a mother with acute HBV disease. 103 Little is known about genetic factors involved in susceptibility to HBV transmission in infancy and early childhood. 101 These infants become positive for HBsAg between 4 and 16 weeks of age and are usually asymptomatic carriers of HBV.…”

“…Age of HBV acquisition is a major determinant of the outcome regarding infection. 103 In addition, genome studies offer another approach to identifying genes involved in disease phenotypes. 102 The modes of transmission include passage of contaminated maternal blood directly from mother to neonate and/or oral inoculation of the neonate by ingestion of maternal blood during birth or at the time of cesarean delivery, and contact with the mother during early infancy by ingestion of contaminated breast milk.…”