Premium
Very low density lipoprotein and low density lipoprotein isolated from patients with hepatitis C infection induce altered cellular lipid metabolism
Author(s) -
Napolitano Mariarosaria,
Giuliani Alessandro,
Alonzi Tonino,
Mancone Carmine,
D'Offizi Gianpiero,
Tripodi Marco,
Bravo Elena
Publication year - 2007
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.20793
Subject(s) - very low density lipoprotein , lipid metabolism , hepatitis c virus , lipoprotein , chemistry , steatosis , metabolism , endocrinology , low density lipoprotein , cholesteryl ester , triglyceride , intermediate density lipoprotein , medicine , biochemistry , cholesterol , biology , virus , immunology
Abstract Several abnormalities of lipid metabolism, including hypo‐β‐lipoproteinemia and liver steatosis are associated with infection by hepatitis C virus (HCV). The aim of this study was to determine whether circulating lipoproteins of patients with HCV infection could directly cause alterations of lipid cellular metabolism. To this end the metabolic response of human monocyte‐derived macrophages (HMDM) to very low‐density lipoprotein (VLDL) and low‐density lipoprotein (LDL), measuring the cholesteryl ester (CE) and triglyceride (TG) production was analyzed. Lipoproteins were isolated from 18 patients infected with hepatitis C virus (HCV‐VLDL and HCV‐LDL) and from normal healthy donors (ct‐VLDL and ct‐LDL). In comparison to ct‐lipoproteins, HCV‐lipoproteins induced significant differences in HMDM CE and TG production. HCV‐VLDL decreased CE and TG production; while HCV‐LDL induced an increased TG synthesis. The present findings suggest that HCV infection modifies VLDL and LDL molecular composition, affecting cellular lipid metabolism, thus promoting intracellular lipid accumulation and hypo‐β‐lipoproteinemia. J. Med. Virol. 79:254–258, 2007. © 2007 Wiley‐Liss, Inc.