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Trends Mol Med. 2015 Jan;21(1):34-42. doi: 10.1016/j.molmed.2014.11.003. Epub 2014 Nov 20.

Hepatitis C virus and lipid droplets: finding a niche.

Author information

1
MRC-University of Glasgow Centre for Virus Research, 464 Bearsden Road, Glasgow G61 1QH, UK.
2
MRC-University of Glasgow Centre for Virus Research, 464 Bearsden Road, Glasgow G61 1QH, UK. Electronic address: john.mclauchlan@glasgow.ac.uk.

Abstract

Hepatitis C virus (HCV) causes serious liver disease in chronically infected individuals. Infectious virions are released from hepatocytes as lipoprotein complexes, indicating that the virus interacts with very low density lipoprotein (VLDL) assembly to propagate. The primary source of lipid for incorporation into VLDL is cytoplasmic lipid droplets (LDs). This organelle is targeted by two virus-encoded proteins as part of a process essential for virion morphogenesis. Moreover, LDs regulate infection. A common condition in HCV-infected individuals is steatosis, characterized by an accumulation of LDs. The mechanisms underlying development of steatosis include direct effects of the virus on lipid metabolism. This review reveals new insights into HCV infection and a further twist to the growing list of functions performed by LDs.

KEYWORDS:

HCV; VLDL; lipid droplets; protein targeting; steatosis; virion assembly

PMID:
25496657
DOI:
10.1016/j.molmed.2014.11.003
[Indexed for MEDLINE]

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