Jump to content
RemedySpot.com

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

Rate this topic


Guest guest

Recommended Posts

http://journals.lww.com/jpgn/Abstract/2011/01000/Hepatitis_B_Virus_Acquisition_a\

nd_Pathogenesis_in.3.aspx

Journal of Pediatric Gastroenterology & Nutrition:

January 2011 - Volume 52 - Issue 1 - p 3–8

doi: 10.1097/MPG.0b013e3181fb0cb9

Review Article

Hepatitis B Virus Acquisition and Pathogenesis in Childhood: Host Genetic

Determinants

Chatzidaki, V*; Kouroumalis, E†; Galanakis, E*

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.

© 2011 Lippincott & Wilkins, Inc.

Link to comment
Share on other sites

http://journals.lww.com/jpgn/Abstract/2011/01000/Hepatitis_B_Virus_Acquisition_a\

nd_Pathogenesis_in.3.aspx

Journal of Pediatric Gastroenterology & Nutrition:

January 2011 - Volume 52 - Issue 1 - p 3–8

doi: 10.1097/MPG.0b013e3181fb0cb9

Review Article

Hepatitis B Virus Acquisition and Pathogenesis in Childhood: Host Genetic

Determinants

Chatzidaki, V*; Kouroumalis, E†; Galanakis, E*

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.

© 2011 Lippincott & Wilkins, Inc.

Link to comment
Share on other sites

Join the conversation

You are posting as a guest. If you have an account, sign in now to post with your account.
Note: Your post will require moderator approval before it will be visible.

Guest
Reply to this topic...

×   Pasted as rich text.   Paste as plain text instead

  Only 75 emoji are allowed.

×   Your link has been automatically embedded.   Display as a link instead

×   Your previous content has been restored.   Clear editor

×   You cannot paste images directly. Upload or insert images from URL.

Loading...
×
×
  • Create New...