Evidence map›Paper›PMID 11714748›Full record

ArticleThe Journal of experimental medicine2001

HIV-1 Vpr enhances viral burden by facilitating infection of tissue macrophages but not nondividing CD4+ T cells.

D A Eckstein, M P Sherman, M L Penn, P S Chin, C M De Noronha, W C Greene, M A Goldsmith

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

62 citing papers in PubMed, 131 citations in OpenAlex.

  1. Article
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  4. Article
  5. Review
  6. Review
  7. Protein ArginineViruses · 2020
    Article
  8. Article
  9. Article
  10. Review
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  13. Article
  14. Article
  15. Article
  16. Article
  17. HIV-1 Viral Protein R Activates NLRP3 Inflammasome in Microglia: implications for HIV-1 Associated Neuroinflammation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2017
    Article
  18. Article
  19. Article
  20. HIV-1 Vpr degrades the HLTF DNA translocase in T cells and macrophages.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article

2 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

D A EcksteinGladstone Institute of Virology and Immunology, University of California San Francisco, San Francisco, CA 94141, USA.
M P Sherman
M L Penn
P S Chin
C M De Noronha
W C Greene
M A Goldsmith
University of California, San Francisco · USGladstone Institutes · US

Funding

UCSF-GIVI CENTER FOR AIDS RESEARCHP30MH059037 · NIMH · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI JACOBSON, MARK A · 1998 to 2001
$4.9M
HIV CORECEPTORS--FUNCTION, SPECIFICITY AND PATHOGENESISR01AI043695 · NIAID · J. DAVID GLADSTONE INSTITUTES · PI GOLDSMITH, MARK A · 1999 to 2001
$570k
ANALYSIS OF HIV VPR ACTION IN LYMPHOID HISTOCULTURESK08AI001866 · NIAID · J. DAVID GLADSTONE INSTITUTES · PI SHERMAN, MICHAEL P · 2001 to 2002
$213k
NIAID NIH HHS K08 AI001866NIAID NIH HHS K08-AI 01866NIAID NIH HHS R01-AI 43695NIMH NIH HHS P30-MH 59037
6 · The paper itself

Abstract

Prior experiments in explants of human lymphoid tissue have demonstrated that human immunodeficiency virus type 1 (HIV-1) productively infects diverse cellular targets including T cells and tissue macrophages. We sought to determine the specific contribution of macrophages and T cells to the overall viral burden within lymphoid tissue. To block infection of macrophages selectively while preserving infection of T cells, we used viruses deficient for viral protein R (Vpr) that exhibit profound replication defects in nondividing cells in vitro. We inoculated tonsil histocultures with matched pairs of congenic viruses that differed only by the presence of a wild-type or truncated vpr gene. Although these viruses exhibited no reduction in the infection or depletion of T cells, the ability of the Vpr-deficient R5 virus to infect tissue macrophages was severely impaired compared with matched wild-type R5 virus. Interestingly, the Vpr-deficient R5 virus also exhibited a 50% reduction in overall virus replication compared with its wild-type counterpart despite the fact that macrophages represent a small fraction of the potential targets of HIV-1 infection in these tissues. Collectively, these data highlight the importance of tissue macrophages in local viral burden and further implicate roles for CC chemokine receptor 5, macrophages, and Vpr in the life cycle and pathogenesis of HIV-1.

Indexed as

Viral LoadCD4-Positive T-LymphocytesCell CycleGene Products, vprHIV-1HumansLymphoid TissueMacrophagesReceptors, CCR5vpr Gene Products, Human Immunodeficiency VirusGene Products, vprReceptors, CCR5vpr Gene Products, Human Immunodeficiency Virus

Identifiers

PMID11714748
PMCPMC2193684
OpenAlexW2117034018

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.