Evidence map›Paper›PMID 22357275›Full record

ArticleJournal of virology2012

Vpu augments the initial burst phase of HIV-1 propagation and downregulates BST2 and CD4 in humanized mice.

Kei Sato, Naoko Misawa, Mitsuko Fukuhara, Shingo Iwami, Dong Sung An, Mamoru Ito, Yoshio Koyanagi

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

46 citing papers in PubMed, 69 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. HIV-1 Vpr hijacks EDD-DYRK2-DDB1The Journal of biological chemistry · 2018
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article
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 at 4 institutions in 2 countries.

Kei SatoCenter for Emerging Virus Research, Kyoto University, Sakyo-ku, Kyoto, Japan.
Naoko Misawa
Mitsuko Fukuhara
Shingo Iwami
Dong Sung An
Mamoru Ito
Yoshio Koyanagi
Kyoto University · JPCentral Institute for Experimental Animals · JPThe University of Tokyo · JPUniversity of California, Los Angeles · US

Funding

Virology CoreP30AI028697 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ANTON, PETER A · 1991 to 2018
$39.9M
NIAID NIH HHS 5P30AI028697NIAID NIH HHS P30 AI028697
6 · The paper itself

Abstract

While human cells express potent antiviral proteins as part of the host defense repertoire, viruses have evolved their own arsenal of proteins to antagonize them. BST2 was identified as an inhibitory cellular protein of HIV-1 replication, which tethers virions to the cell surface to prevent their release. On the other hand, the HIV-1 accessory protein, Vpu, has the ability to downregulate and counteract BST2. Vpu also possesses the ability to downmodulate cellular CD4 and SLAMF6 molecules expressed on infected cells. However, the role of Vpu in HIV-1 infection in vivo remains unclear. Here, using a human hematopoietic stem cell-transplanted humanized mouse model, we demonstrate that Vpu contributes to the efficient spread of HIV-1 in vivo during the acute phase of infection. Although Vpu did not affect viral cytopathicity, target cell preference, and the level of viral protein expression, the amount of cell-free virions in vpu-deficient HIV-1-infected mice was profoundly lower than that in wild-type HIV-1-infected mice. We provide a novel insight suggesting that Vpu concomitantly downregulates BST2 and CD4, but not SLAMF6, from the surface of infected cells. Furthermore, we show evidence suggesting that BST2 and CD4 impair the production of cell-free infectious virions but do not associate with the efficiency of cell-to-cell HIV-1 transmission. Taken together, our findings suggest that Vpu downmodulates BST2 and CD4 in infected cells and augments the initial burst of HIV-1 replication in vivo. This is the first report demonstrating the role of Vpu in HIV-1 infection in an in vivo model.

Indexed as

Down-RegulationAnimalsAntigens, CDBone Marrow Stromal Antigen 2CD4 AntigensCell CommunicationCell LineCell MembraneGene Expression ProfilingHIV-1HIV InfectionsHuman Immunodeficiency Virus ProteinsHumansMembrane GlycoproteinsMiceMice, Inbred NODAntigens, CDBone Marrow Stromal Antigen 2BST2 protein, mouseCD4 AntigensHuman Immunodeficiency Virus ProteinsMembrane GlycoproteinsViral Regulatory and Accessory ProteinsViroporin Proteinsvpu protein, Human immunodeficiency virus 1

Identifiers

PMID22357275
PMCPMC3347374
OpenAlexW1990945574

What OpenQuestion holds

Textmetadata
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.