Evidence map›Paper›PMID 20550452›Full record

ArticleClinical infectious diseases : an official publication of the Infectious Diseases Society of America2010

Infrequent recovery of HIV from but robust exogenous infection of activated CD4(+) T cells in HIV elite controllers.

B Julg, F Pereyra, M J Buzón, A Piechocka-Trocha, M J Clark, B M Baker, J Lian, T Miura, J Martinez-Picado, M M Addo and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Clinical infectious diseases : an official publication of the Infectious Diseases Society of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

84 citing papers in PubMed, 108 citations in OpenAlex.

  1. Trial
  2. Article
  3. The HIV reservoir landscape in elite controllers.Current opinion in HIV and AIDS · 2026
    Review
  4. Article
  5. Engineering of CD8mBio · 2025
    Article
  6. Review
  7. Antigen Presenting Cell-Mediated HIV-1Medical research archives · 2023
    Article
  8. Review
  9. Article
  10. Article
  11. Molecular Biology and Diversification of Human Retroviruses.Frontiers in virology (Lausanne, Switzerland) · 2022
    Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. The role of CD38 in HIV infection.AIDS research and therapy · 2021
    Review
  17. Article
  18. Article
  19. Review
  20. CD8Frontiers in microbiology · 2021
    Article

24 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

11 authors at 3 institutions in 2 countries.

B JulgRagon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology and Harvard, Boston, Massachusetts, USA.
F Pereyra
M J Buzón
A Piechocka-Trocha
M J Clark
B M Baker
J Lian
T Miura
J Martinez-Picado
M M Addo
B D Walker
Ragon Institute of MGH, MIT and Harvard · USHospital Universitari Germans Trias i Pujol · ESHoward Hughes Medical Institute · US

Funding

The impact of HIV viral diversity and cellular immunity on HIV pathogenesisP30AI060354 · NIAID · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI Daniel Lingwood · 2004 to 2026
$94.4M
INHIBITION OF HIV1 REPLICATION BY CYTOTOXIC LYMPHOCYTESR01AI030914 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI WALKER, BRUCE D · 1991 to 2013
$4.2M
NIAID NIH HHS P30 AI060354NIAID NIH HHS R01 AI030914
6 · The paper itself

Abstract

BACKGROUND. Human immunodeficiency virus (HIV) elite controllers are able to control infection with HIV-1 spontaneously to undetectable levels in the absence of antiretroviral therapy, but the mechanisms leading to this phenotype are poorly understood. Although low frequencies of HIV-infected peripheral CD4(+) T cells have been reported in this group, it remains unclear to what extent these are due to viral attenuation, active immune containment, or intracellular host factors that restrict virus replication. METHODS. We assessed proviral DNA levels, autologous viral growth from and infectability of in vitro activated, CD8(+) T cell-depleted CD4(+) T cells from HIV elite controllers (mean viral load, <50 copies/mL), viremic controllers (mean viral load, <2000 copies/mL), chronic progressors, and individuals receiving highly active antiretroviral therapy. RESULTS. Although we successfully detected autologous virus production in ex vivo activated CD4(+) T cells from all chronic progressors and from most of the viremic controllers, we were able to measure robust autologous viral replication in only 2 of 14 elite controllers subjected to the same protocol. In vitro activated autologous CD4(+) T cells from elite controllers, however, supported infection with both X4 and R5 tropic HIV strains at comparable levels to those in CD4(+) T cells from HIV-uninfected subjects. Proviral DNA levels were the lowest in elite controllers, suggesting that extremely low frequencies of infected cells contribute to difficulty in isolation of virus. CONCLUSIONS. These data indicate that elite control is not due to inability of activated CD4(+) T cells to support HIV infection, but the relative contributions of host and viral factors that account for maintenance of low-level infection remain to be determined.

Indexed as

HIV Long-Term SurvivorsCD4-Positive T-LymphocytesCells, CulturedHIV-1HIV InfectionsHumansVirulenceVirus Replication

Identifiers

PMID20550452
PMCPMC3749734
OpenAlexW1989633434

What OpenQuestion holds

Textmetadata
LicenceTDM
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.