ArticleThe Journal of general virology2006
Preferential association of Hepatitis C virus with apolipoprotein B48-containing lipoproteins.
Article in The Journal of general virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 99 citations in OpenAlex.
- Nicotinamide metabolism is essential for Hepatitis C Virus replication and the production of infectious Lipo-Viro-Particles.PLoS pathogens · 2026Article
- Cellular factors involved in the hepatitis C virus life cycle.World journal of gastroenterology · 2021Review
- Hepatitis C Virus Uses Host Lipids to Its Own Advantage.Metabolites · 2021Review
- HCV Assembly and Egress via Modifications in Host Lipid Metabolic Systems.Cold Spring Harbor perspectives in medicine · 2021Review
- Role of RNA-binding proteins during the late stages of Flavivirus replication cycle.Virology journal · 2020Review
- Review
- Rapid Changes in Serum Lipid Profiles during Combination Therapy with Daclatasvir and Asunaprevir in Patients Infected with Hepatitis C Virus Genotype 1b.Gut and liver · 2018Article
- Hepatitis C virus-apolipoprotein interactions: molecular mechanisms and clinical impact.Expert review of proteomics · 2017Review
- Review
- Article
- Hepatitis C virus G1b infection decreases the number of small low-density lipoprotein particles.World journal of gastroenterology · 2016Article
- Distinct Roles for Intracellular and Extracellular Lipids in Hepatitis C Virus Infection.PloS one · 2016Article
- Targeting host lipid synthesis and metabolism to inhibit dengue and hepatitis C viruses.Antiviral research · 2015Review
- Modulation of host lipid metabolism by hepatitis C virus: Role of new therapies.World journal of gastroenterology · 2015Review
- Chronic hepatitis C virus infection and lipoprotein metabolism.World journal of gastroenterology · 2015Review
- Proteomic approaches to analyzing hepatitis C virus biology.Proteomics · 2015Review
- AP-2-associated protein kinase 1 and cyclin G-associated kinase regulate hepatitis C virus entry and are potential drug targets.Journal of virology · 2015Article
- Impact of lipids and lipoproteins on hepatitis C virus infection and virus neutralization.World journal of gastroenterology · 2014Review
- Plasma triglyceride levels may modulate hepatitis C viral replication.Digestive diseases and sciences · 2014Article
- Incorporation of hepatitis C virus E1 and E2 glycoproteins: the keystones on a peculiar virion.Viruses · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis C virus (HCV) in cell culture has a density comparable to that of other members of the family Flaviviridae, whereas in vivo infectious particles are found partially in low-density fractions, associated with triacylglycerol (TG)-rich lipoproteins (TRLs). In the blood of infected patients, HCV circulates as heterogeneous particles, among which are lipo-viroparticles (LVPs), globular particles rich in TG and containing viral capsid and RNA. The dual viral and lipoprotein nature of LVPs was addressed further with respect to apolipoprotein composition and post-prandial dynamic lipid changes. The TRLs exchangeable apoE, -CII and -CIII, but not the high-density lipoprotein apoA-II, were present on LVPs, as well as the viral envelope proteins. apoB100 and -B48, the two isoforms of the non-exchangeable apoB, were represented equally on LVPs, despite the fact that apoB48 was barely detectable in the plasma of these fasting patients. This indicates that a significant fraction of plasma HCV was associated with apoB48-containing LVPs. Furthermore, LVPs were enriched dramatically and rapidly in triglycerides after a fat meal. As apoB48 is synthesized exclusively by the intestine, these data highlight the preferential association of HCV with chylomicrons, the intestine-derived TRLs. These data raise the question of the contribution of the intestine to the viral load and suggest that the virus could take advantage of TRL assembly and secretion for its own production and of TRL fate to be delivered to the liver.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.