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Review
. 2017 Jul 28;10(1):17-20.
doi: 10.1002/cld.643. eCollection 2017 Jul.

Lipid interactions influence hepatitis C virus susceptibility and resistance to infection

Isaac Thom Shawa  1 , David A Sheridan  1   2 , Daniel J Felmlee  1 , Matthew E Cramp  1   2
Affiliations
Review

Lipid interactions influence hepatitis C virus susceptibility and resistance to infection

Isaac Thom Shawa et al. Clin Liver Dis (Hoboken). .
No abstract available

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Figures

Figure 1
Figure 1
HCV life cycle. (1) HCV circulates in the blood as LVPs. (2) The LVP leaves the circulation through fenestrated endothelia and accesses the hepatocytes via the space of Disse. The LVP interacts with host cell receptor molecules such as heparan sulfate glycosaminoglycan (HS‐GAG), low‐density lipoprotein receptor (LDLR), and others with high affinity for apolipoproteins. (3) The LVP then binds to entry factors enabling clathrin‐mediated endocytosis. (4) Uncoating of viral capsid delivers viral genomic material to cytoplasmic replication site. (5) Successful viral entry through lipoprotein channels leads to translation of polypeptides in endoplasmic reticulum. (6) Replication complex forms +ssRNA strands via −ssRNA intermediates in membranous web, which shows characteristics of lipid rafts. (7) Virions assemble and bud through lipid channels that secrete mature virions via VLDL pathway. (8) Mature virions are released from the cell. LD, lipid droplet; RER, rough endoplasmic reticulum.
Figure 2
Figure 2
Schematic model of an HCV LVP. HCV circulates in the blood in association with host lipoproteins in a complex called a LVP that contains both viral (envelope, core, RNA) and host lipoprotein constituents including cholesterol, triglycerides, apoB, apoE, and apoC1.2 LVPs are important in HCV attachment and entry, and may mask viral epitopes from antibody‐mediated neutralization.
Figure 3
Figure 3
Lipidomics. Multivariate analysis using principal component analysis and OPLS‐DA for HCV‐resistant cases (EU, n = 38) compared with HCV‐susceptible (HCV antibody‐positive, n = 295), including chronic HCV patients genotypes 1 or 3 (HCV RNA‐positive, n = 159), SVRs (n = 100), and SRs (n = 36). Summary of data presented as poster 15 at the BASL Annual Meeting 2016.10
See this image and copyright information in PMC

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