Animal models of HBV infection

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Animal models of HBV infection. / Dandri, Maura; Petersen, Joerg.

In: BEST PRACT RES CL GA, Vol. 31, No. 3, 06.2017, p. 273-279.

Research output: SCORING: Contribution to journalSCORING: Review articleResearch

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@article{ea041420cb1b479d92340555074a96d0,
title = "Animal models of HBV infection",
abstract = "The mechanisms determining hepatitis B virus (HBV) persistence and pathogenesis are not fully elucidated, but appear to be multi-factorial. Current medication to repress viral replication is available; however, the unique replication strategies employed by HBV enable the virus to persist within the infected hepatocytes. Consequently, cure is rarely achieved. Progresses in HBV research and preclinical testing of antiviral agents have been limited by the narrow species- and tissue-tropism of the virus, the paucity of infection models available and the restrictions imposed by the use of chimpanzees, the only animals fully susceptible to HBV infection. Mice are not HBV permissive but major efforts have focused on the development of mouse models of HBV replication and infection, such as the generation of humanized mice. By presenting the different animal models available, this review will highlight the most important and clinically relevant findings that have been retrieved from the respective systems.",
keywords = "Journal Article, Review",
author = "Maura Dandri and Joerg Petersen",
note = "Copyright {\textcopyright} 2017 Elsevier Ltd. All rights reserved.",
year = "2017",
month = jun,
doi = "10.1016/j.bpg.2017.04.014",
language = "English",
volume = "31",
pages = "273--279",
journal = "BEST PRACT RES CL GA",
issn = "1521-6918",
publisher = "Bailliere Tindall Ltd",
number = "3",

}

RIS

TY - JOUR

T1 - Animal models of HBV infection

AU - Dandri, Maura

AU - Petersen, Joerg

N1 - Copyright © 2017 Elsevier Ltd. All rights reserved.

PY - 2017/6

Y1 - 2017/6

N2 - The mechanisms determining hepatitis B virus (HBV) persistence and pathogenesis are not fully elucidated, but appear to be multi-factorial. Current medication to repress viral replication is available; however, the unique replication strategies employed by HBV enable the virus to persist within the infected hepatocytes. Consequently, cure is rarely achieved. Progresses in HBV research and preclinical testing of antiviral agents have been limited by the narrow species- and tissue-tropism of the virus, the paucity of infection models available and the restrictions imposed by the use of chimpanzees, the only animals fully susceptible to HBV infection. Mice are not HBV permissive but major efforts have focused on the development of mouse models of HBV replication and infection, such as the generation of humanized mice. By presenting the different animal models available, this review will highlight the most important and clinically relevant findings that have been retrieved from the respective systems.

AB - The mechanisms determining hepatitis B virus (HBV) persistence and pathogenesis are not fully elucidated, but appear to be multi-factorial. Current medication to repress viral replication is available; however, the unique replication strategies employed by HBV enable the virus to persist within the infected hepatocytes. Consequently, cure is rarely achieved. Progresses in HBV research and preclinical testing of antiviral agents have been limited by the narrow species- and tissue-tropism of the virus, the paucity of infection models available and the restrictions imposed by the use of chimpanzees, the only animals fully susceptible to HBV infection. Mice are not HBV permissive but major efforts have focused on the development of mouse models of HBV replication and infection, such as the generation of humanized mice. By presenting the different animal models available, this review will highlight the most important and clinically relevant findings that have been retrieved from the respective systems.

KW - Journal Article

KW - Review

U2 - 10.1016/j.bpg.2017.04.014

DO - 10.1016/j.bpg.2017.04.014

M3 - SCORING: Review article

C2 - 28774409

VL - 31

SP - 273

EP - 279

JO - BEST PRACT RES CL GA

JF - BEST PRACT RES CL GA

SN - 1521-6918

IS - 3

ER -