ArticlePloS one2014
HIV-1 Nef is transferred from expressing T cells to hepatocytic cells through conduits and enhances HCV replication.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 24 citations in OpenAlex.
- HIV-1-related factors interact with p53 to influence cellular processes.AIDS research and therapy · 2023Review
- Novel role of HIV-1 Nef in regulating the ubiquitination of cellular proteins.Frontiers in cellular and infection microbiology · 2023Article
- Review
- Oncogenic Effects of HIV-1 Proteins, Mechanisms Behind.Cancers · 2021Review
- A Tale of Two Viruses: Immunological Insights Into HCV/HIV Coinfection.Frontiers in immunology · 2021Review
- The role of MDM2-p53 axis dysfunction in the hepatocellular carcinoma transformation.Cell death discovery · 2020Review
- Characterization of Nef expression in different brain regions of SIV-infected macaques.PloS one · 2020Article
- Alcohol Metabolism Potentiates HIV-Induced Hepatotoxicity: Contribution to End-Stage Liver Disease.Biomolecules · 2019Article
- HIV-1 Impairment via UBE3A and HIV-1 Nef Interactions Utilizing the Ubiquitin Proteasome System.Viruses · 2019Article
- Nef-induced CCL2 Expression Contributes to HIV/SIV Brain Invasion and Neuronal Dysfunction.Frontiers in immunology · 2019Review
- Positive-sense RNA viruses reveal the complexity and dynamics of the cellular and viral epitranscriptomes during infection.Nucleic acids research · 2018Article
- Consequence of HIV and HCV co-infection on host immune response, persistence and current treatment options.Virusdisease · 2018Review
- [Advances in application of Jurkat cell model in research on infectious diseases].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2018Review
- Signature molecules expressed differentially in a liver disease stage-specific manner by HIV-1 and HCV co-infection.PloS one · 2018Article
- Function of ubiquitin (Ub) specific protease 15 (USP15) in HIV-1 replication and viral protein degradation.Virus research · 2016Article
- HIV Vpr protein upregulates microRNA-122 expression and stimulates hepatitis C virus replication.The Journal of general virology · 2015Article
- Virological Mechanisms in the Coinfection between HIV and HCV.Mediators of inflammation · 2015Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
HIV-1 infection enhances HCV replication and as a consequence accelerates HCV-mediated hepatocellular carcinoma (HCC). However, the precise molecular mechanism by which this takes place is currently unknown. Our data showed that infectious HIV-1 failed to replicate in human hepatocytic cell lines. No discernible virus replication was observed, even when the cell lines transfected with HIV-1 proviral DNA were co-cultured with Jurkat T cells, indicating that the problem of liver deterioration in the co-infected patient is not due to the replication of HIV-1 in the hepatocytes of the HCV infected host. Instead, HIV-1 Nef protein was transferred from nef-expressing T cells to hepatocytic cells through conduits, wherein up to 16% (average 10%) of the cells harbored the transferred Nef, when the hepatocytic cells were co-cultured with nef-expressing Jurkat cells for 24 h. Further, Nef altered the size and numbers of lipid droplets (LD), and consistently up-regulated HCV replication by 1.5∼2.5 fold in the target subgenomic replicon cells, which is remarkable in relation to the initially indolent viral replication. Nef also dramatically augmented reactive oxygen species (ROS) production and enhanced ethanol-mediated up-regulation of HCV replication so as to accelerate HCC. Taken together, these data indicate that HIV-1 Nef is a critical element in accelerating progression of liver pathogenesis via enhancing HCV replication and coordinating modulation of key intra- and extra-cellular molecules for liver decay.
Indexed as
Identifiers
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.