Abstract | OBJECTIVE: DESIGN: RESULTS: A higher triglyceride/ cholesterol ratio of LDL was found more in HCV-infected donors than in healthy volunteers, and the triglyceride/ cholesterol ratio of LDL-LVP was much increased, suggesting that the LPL hydrolysis of triglyceride may be impaired. VLDL, VLDL-LVP, LDL-LVP, but not LDL, suppressed LPL lipolytic activity, which was restored by antibodies that recognised apoC-III/-IV and correlated with the steadily abundant apoC-III/-IV quantities in those particles. In a cell-based system, treatment with VLDL and LVPs reversed the LPL-mediated inhibition of HCV infection in apoC-III/-IV-dependent manners. A multivariate logistic regression revealed that plasma HCV viral loads correlated negatively with LPL lipolytic activity, but positively with the apoC-III content of VLDL. Additionally, apoC-III in VLDL was associated with a higher proportion of HCV- RNA than was IgG. CONCLUSION: This study reveals that LPL is an anti-HCV factor, and that apoC-III in VLDL and LVPs reduces the LPL-mediated inhibition of HCV infection.
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Authors | Hung-Yu Sun, Chun-Chieh Lin, Jin-Ching Lee, Shainn-Wei Wang, Pin-Nan Cheng, I-Chin Wu, Ting-Tsung Chang, Ming-Derg Lai, Dar-Bin Shieh, Kung-Chia Young |
Journal | Gut
(Gut)
Vol. 62
Issue 8
Pg. 1193-203
(Aug 2013)
ISSN: 1468-3288 [Electronic] England |
PMID | 22689516
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Apolipoprotein C-III
- Lipoproteins, LDL
- Lipoproteins, VLDL
- Triglycerides
- Cholesterol
- Lipoprotein Lipase
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Topics |
- Adult
- Apolipoprotein C-III
(physiology)
- Blood Donors
- Cells, Cultured
- Cholesterol
(blood)
- Female
- Hepacivirus
(isolation & purification, metabolism, pathogenicity)
- Hepatitis C, Chronic
(blood, virology)
- Humans
- Lipolysis
(physiology)
- Lipoprotein Lipase
(physiology)
- Lipoproteins, LDL
(blood)
- Lipoproteins, VLDL
(blood, physiology)
- Male
- Triglycerides
(blood)
- Viral Load
- Virion
(metabolism)
- Virulence
(physiology)
- Young Adult
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