Evidence map›Paper›PMID 28722331›Full record

ReviewJournal of cellular and molecular medicine2017

Hepatitis C virus and proprotein convertase subtilisin/kexin type 9: a detrimental interaction to increase viral infectivity and disrupt lipid metabolism.

Matteo Pirro, Vanessa Bianconi, Daniela Francisci, Elisabetta Schiaroli, Francesco Bagaglia, Amirhossein Sahebkar, Franco Baldelli

Abstract readReview
In one paragraph

Review in Journal of cellular and molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Evaluation of Proteomic and Lipidomic Changes inInternational journal of molecular sciences · 2022
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Matteo PirroUnit of Internal Medicine, Department of Medicine, University of Perugia, Perugia, Italy.ORCID http://orcid.org/0000-0002-5527-4821
Vanessa BianconiUnit of Internal Medicine, Department of Medicine, University of Perugia, Perugia, Italy.
Daniela FrancisciUnit of Infectious Diseases, Department of Medicine, University of Perugia, Perugia, Italy.
Elisabetta SchiaroliUnit of Infectious Diseases, Department of Medicine, University of Perugia, Perugia, Italy.
Francesco BagagliaUnit of Internal Medicine, Department of Medicine, University of Perugia, Perugia, Italy.
Amirhossein SahebkarBiotechnology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Franco BaldelliUnit of Infectious Diseases, Department of Medicine, University of Perugia, Perugia, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

From viral binding to the hepatocyte surface to extracellular virion release, the replication cycle of the hepatitis C virus (HCV) intersects at various levels with lipid metabolism; this leads to a derangement of the lipid profile and to increased viral infectivity. Accumulating evidence supports the crucial regulatory role of proprotein convertase subtilisin/kexin type 9 (PCSK9) in lipoprotein metabolism. Notably, a complex interaction between HCV and PCSK9 has been documented. Indeed, either increased or reduced circulating PCSK9 levels have been observed in HCV patients; this discrepancy might be related to several confounders, including HCV genotype, human immunodeficiency virus (HIV) coinfection and the ambiguous HCV-mediated influence on PCSK9 transcription factors. On the other hand, PCSK9 may itself influence HCV infectivity, inasmuch as the expression of different hepatocyte surface entry proteins and receptors is regulated by PCSK9. The aim of this review is to summarize the current evidence about the complex interaction between HCV and liver lipoprotein metabolism, with a specific focus on PCSK9. The underlying assumption of this review is that the interconnections between HCV and PCSK9 may be central to explain viral infectivity.

Indexed as

Host-Pathogen InteractionsGene Expression RegulationGenotypeHepacivirusHepatitis C, ChronicHepatocytesHumansLipid MetabolismProprotein Convertase 9Receptors, LipoproteinReceptors, VirusSignal TransductionViral ProteinsVirulenceVirus ReplicationPCSK9 protein, humanProprotein Convertase 9Receptors, LipoproteinReceptors, VirusViral Proteinscholesterolhepatitis C viruslipidslipoproteinproprotein convertase subtilisin/kexin type 9

Identifiers

PMID28722331
PMCPMC5706572

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Registered trials

None linked

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.