Editorial
Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. Apr 28, 2015; 7(6): 819-824
Published online Apr 28, 2015. doi: 10.4254/wjh.v7.i6.819
Role natural killer group 2D-ligand interactions in hepatitis B infection
Teresa Pollicino, Lemonica Koumbi
Teresa Pollicino, Department of Pediatric, Gynecologic, Microbiologic, and Biomedical Sciences, University Hospital of Messina, 98124 Messina, Italy
Lemonica Koumbi, Department of Medicine, Hepatology and Gastroenterology Section, Imperial College, St. Mary’s Campus, W2 1PG London, United Kingdom
Author contributions: Pollicino T and Koumbi L contributed to this paper.
Conflict-of-interest: I accept responsibility for the contents of the amended manuscript and I affirm that there is no conflict of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Lemonica Koumbi, Research Fellow, Department of Medicine, Hepatology and Gastroenterology Section, Imperial College, St. Mary’s Campus, Norfolk Place, W2 1PG London, United Kingdom. lemonica.koumbi@gmail.com
Telephone: +44-207-5949022 Fax: +44-207-7069161
Received: January 28, 2015
Peer-review started: January 28, 2015
First decision: February 7, 2015
Revised: February 17, 2015
Accepted: March 16, 2015
Article in press: March 18, 2015
Published online: April 28, 2015
Processing time: 93 Days and 12.4 Hours
Abstract

Hepatitis B virus (HBV) infection is the leading cause of liver disease and hepatocellular carcinoma (HCC) worldwide, in spite of prophylactic vaccination and antiviral treatment modalities. The immunopathogenesis of HBV infection has been intensively studied and is propelled by complex interactions between the virus and the host immune system. Natural killer group 2D (NKG2D) is a well-characterized activating receptor, expressed on natural killer (NK) cells, NK T cells and CD8+ cytotoxic T cells. This receptor is present in both humans and mice and binds to a diverge family of ligands that resemble the MHC-class I molecules. Increasing evidence shows that NKG2D-ligand interactions are critical in the establishment of HBV persistence and the development of liver injury and HCC. The expression of NKG2D ligands depends on the presence of several polymorphisms and is also modulated post-transcriptionally by HBV. While it is known that HBV circumvents host’s innate immunity via the NKG2D pathway but the exact mechanisms involved are still elusive. This letter discusses previous accomplishments on the role of NKG2D ligand regulation in the development of chronic HBV, liver injury and HCC.

Keywords: Hepatitis B virus; Natural killer group 2D receptor; Natural killer cells; MHC class I polypeptide-related chain A; Hepatocellular carcinoma

Core tip: Hepatitis B virus (HBV) infection is the leading cause of liver disease and hepatocellular carcinoma (HCC) worldwide. HBV persistence involves complex interactions between the virus and the immune system of the host. Natural killer group 2D (NKG2D) is an activating receptor, expressed on natural killer (NK), NK T and CD8+ T cells. NKG2D-ligand interactions are critical in the establishment of chronicity and the development of liver injury and HCC. However, the exact mechanisms involved are still elusive. Here previous studies are discussed on how HBV modulates the NKG2D activity to result in viral clearance, susceptibility to liver injury and tumour evasion.