Journal
JOURNAL OF GENERAL VIROLOGY
Volume 97, Issue -, Pages 121-127Publisher
SOC GENERAL MICROBIOLOGY
DOI: 10.1099/jgv.0.000317
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Funding
- National Institute for Health Research Birmingham Liver Biomedical Research Unit
- Medical Research Council [G1100247]
- EU FP7 funded PathCO HEALTH [F3-2012-305578, ERC-2013-StG 337479]
- Technische Universitat Munchen - Institute for Advanced Study - German Excellence Initiative
- European Union Seventh Framework Programme [291763]
- Netherlands Organization for Health Research and Development [Vidi 91713319]
- Chinese Scholarship Council
- BBSRC [BB/N008553/1] Funding Source: UKRI
- MRC [G0801976, G0400802, G1100247] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/N008553/1] Funding Source: researchfish
- Medical Research Council [G0801976, G0400802] Funding Source: researchfish
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Hepatitis B virus (HBV) is one of the world's major unconquered infections, resulting in progressive liver disease, and current treatments rarely cure infection. A limitation to discovering new therapies is our limited knowledge of HBV entry and dissemination pathways that hinders the development of in vitro culture systems. To address this gap in our understanding we optimized the genesis of infectious lentiviral pseudoparticles (HBVpps). The recent discovery that the bile salt transporter sodium taurocholate co-transporting polypeptide (NTCP) acts as a receptor for HBV enabled us to assess the receptor dependency of HBVpp infection. HBVpps preferentially infect hepatoma cells expressing NTCP, whereas other non-liver cells engineered to express NTCP do not support infection, suggesting that additional hepatocyte-specific factors are required for HBVpp internalization. These results highlight the value of the HBVpp system to dissect the pathways of HBV entry and dissemination.
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