Evidence map›Paper›PMID 31431548›Full record

ArticlemBio2019

Vpr Enhances HIV-1 Env Processing and Virion Infectivity in Macrophages by Modulating TET2-Dependent IFITM3 Expression.

Qi Wang, Lishan Su

Open access · goldAbstract read
In one paragraph

Article in mBio, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.6field-weighted citation impact, top 9% of its field
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

24 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Article
  3. The HIV-1 Vpr R77Q mutant alters host apoptotic gene regulation in CD4+ T cells.Frontiers in cellular and infection microbiology · 2026
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Deciphering DNA Methylation in HIV Infection.Frontiers in immunology · 2021
    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

2 authors at 1 institution in 1 country.

Qi WangLineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Lishan SuLineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA lsu@med.unc.edu.
University of North Carolina at Chapel Hill · US

Funding

Blocking type I interferon signaling to reverse T cell exhaustion and control HIV-1 reservoirsR01AI136990 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI AMARA, RAMA RAO, BOSINGER, STEVEN EDWARD · 2018 to 2022
$4.2M
HIV-1 Vpr disrupts the IFN-TET-ISG pathway to promote HIV-1 infection and persistenceR01AI127346 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SU, LISHAN · 2016 to 2020
$2.7M
Immune Mechanisms of Elevated Liver Diseases During HIV InfectionR01DK119937 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SU, LISHAN · 2018 to 2022
$1.9M
NIAID NIH HHS R01 AI127346NIAID NIH HHS R01 AI136990NIDDK NIH HHS R01 DK119937
6 · The paper itself

Abstract

HIV-1 Vpr enhances viral replication in human macrophages via multiple mechanisms that are not clearly defined. It does not affect HIV-1 virion production during the first round of infection. We have recently discovered that Vpr targets the DNA demethylase TET2 for degradation, which leads to sustained interleukin-6 (IL-6) expression and elevated HIV-1 replication. We report here that Vpr enhanced Env processing in infected macrophages, associated with increased Env incorporation into virions with higher infectivity. Interestingly, IFITM3 was constitutively expressed in macrophages in a TET2-dependent fashion. We showed that Vpr-enhanced Env processing depended genetically on TET2 and IFITM3. We further showed that Vpr reduced IFITM3 expression by reducing demethylation of the IFITM3 promoter in macrophages, associated with degradation of TET2 and reduced TET2 binding to the IFITIM3 promoter. Our findings indicate that the Vpr-TET2 axis enhances HIV-1 replication in macrophages via two independent mechanisms: reduced IFTIM3 expression to enhance Env processing and virion infectivity and sustained IL-6 expression to increase HIV-1 replication. The Vpr-TET2 axis may provide a novel target to develop therapeutics to inhibit HIV-1 infection and pathogenesis.

Indexed as

Anti-HIV AgentsCarrier ProteinsCell LineDioxygenasesDNA-Binding ProteinsDNA Demethylationenv Gene Products, Human Immunodeficiency VirusGene Expression Regulation, ViralHIV-1HumansInterleukin-6MacrophagesMembrane ProteinsPromoter Regions, GeneticProto-Oncogene ProteinsRNA-Binding ProteinsAnti-HIV AgentsCarrier ProteinsDioxygenasesDNA-Binding Proteinsenv Gene Products, Human Immunodeficiency VirusIFITM3 protein, humanInterleukin-6Membrane ProteinsProto-Oncogene ProteinsRNA-Binding ProteinsTET2 protein, humanvpr Gene Products, Human Immunodeficiency VirusdemethylationEnv processingHIV-1 infectivityIFITM3TET2Vpr

Identifiers

PMID31431548
PMCPMC6703422
OpenAlexW2969404469

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.