P0691 : Knockdown of lysophosphatidylcholine acyltransferase 1 (LPCAT1) increases both the secretion of very-low-density lipoproteins (VLDL) and the infectivity of hepatitis C virus (HCV)

2015 ◽  
Vol 62 ◽  
pp. S581
Author(s):  
M. Lemasson ◽  
F. Beilstein ◽  
V. Pène ◽  
A.R. Rosenberg ◽  
S. Demignot
2007 ◽  
Vol 82 (5) ◽  
pp. 2120-2129 ◽  
Author(s):  
Pablo Gastaminza ◽  
Guofeng Cheng ◽  
Stefan Wieland ◽  
Jin Zhong ◽  
Wei Liao ◽  
...  

ABSTRACT Intracellular infectious hepatitis C virus (HCV) particles display a distinctly higher buoyant density than do secreted virus particles, suggesting that the characteristic low density of extracellular HCV particles is acquired during viral egress. We took advantage of this difference to examine the determinants of assembly, maturation, degradation, and egress of infectious HCV particles. The results demonstrate that HCV assembly and maturation occur in the endoplasmic reticulum (ER) and post-ER compartments, respectively, and that both depend on microsomal transfer protein and apolipoprotein B, in a manner that parallels the formation of very-low-density lipoproteins (VLDL). In addition, they illustrate that only low-density particles are efficiently secreted and that immature particles are actively degraded, in a proteasome-independent manner, in a post-ER compartment of the cell. These results suggest that by coopting the VLDL assembly, maturation, degradation, and secretory machinery of the cell, HCV acquires its hepatocyte tropism and, by mimicry, its tendency to persist.


2009 ◽  
Vol 90 (5) ◽  
pp. 1055-1070 ◽  
Author(s):  
Michela E. Burlone ◽  
Agata Budkowska

Hepatitis C virus (HCV), a major cause of chronic liver disease, is a single-stranded positive sense virus of the family Flaviviridae. HCV cell entry is a multi-step process, involving several viral and cellular factors that trigger virus uptake into the hepatocyte. Tetraspanin CD81, human scavenger receptor SR-BI, and tight junction molecules Claudin-1 and occludin are the main receptors that mediate HCV entry. In addition, the virus may use glycosaminoglycans and/or low density receptors on host cells as initial attachment factors. A unique feature of HCV is the dependence of virus replication and assembly on host cell lipid metabolism. Most notably, during HCV assembly and release from the infected cells, virus particles associate with lipids and very-low-density lipoproteins. Thus, infectious virus circulates in patient sera in the form of triglyceride-rich particles. Consequently, lipoproteins and lipoprotein receptors play an essential role in virus uptake and the initiation of infection. This review summarizes the current knowledge about HCV receptors, mechanisms of HCV cell entry and the role of lipoproteins in this process.


Gut ◽  
2010 ◽  
Vol 60 (3) ◽  
pp. 378-386 ◽  
Author(s):  
C. Mancone ◽  
C. Steindler ◽  
L. Santangelo ◽  
G. Simonte ◽  
C. Vlassi ◽  
...  

1969 ◽  
Vol 244 (20) ◽  
pp. 5687-5694 ◽  
Author(s):  
W. Virgil Brown ◽  
Robert I. Levy ◽  
Donald S. Fredrickson

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