Evidence map›Paper›PMID 17411338›Full record

Trial reportPLoS pathogens2007

ART suppresses plasma HIV-1 RNA to a stable set point predicted by pretherapy viremia.

Frank Maldarelli, Sarah Palmer, Martin S King, Ann Wiegand, Michael A Polis, JoAnn Mican, Joseph A Kovacs, Richard T Davey, Diane Rock-Kress, Robin Dewar and 8 more

3 registry-linked trialsAbstract readClinical Trial, Phase IIIRandomized Controlled Trial
In one paragraph

Trial report in PLoS pathogens, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 3 registered trials, which are not on this map. Cited by 219 papers.

0numbers the graph read from it
0cells of the map it votes in
219citing papers in PubMed
–field-weighted citation impact
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.

NCT00618371 nacompletednot on this map

Investigating the Source of HIV-1 Viremia in Patients on Antiretroviral Therapy Through Intensification With MK-0518

TypeinterventionalSponsorUniversity of PittsburghRan2007 to 2009Enrolled10ConditionsHIV InfectionArmsRaltegravir (MK-0518)
NCT01295515 phase1 / phase2completednot on this mapstarted 2011, after this paper: background citation

Effect of Interferon Alpha 2b Intensification on HIV-1 Residual Viremia in Individuals Suppressed on Antiretroviral Therapy

TypeinterventionalSponsorNational Cancer Institute (NCI)Ran2011 to 2017Enrolled7ConditionsHIV InfectionArmsPegylated Interferon Alpha 2b (PEGINTRON)
NCT02042248 phase1completednot on this mapstarted 2014, after this paper: background citation

IGHID 1309 -A Phase I Study to Evaluate the Kinetics of the Immunologic Response and Virologic Impact of AGS-004 in HIV-Infected Individuals Suppressed on Antiretroviral Therapy Initiated During Acute and Chronic HIV Infection

TypeinterventionalSponsorCynthia L Gay, MDRan2014 to 2016Enrolled6ConditionsHIVArmsAGS-004
3 · Its place in the literature

Who cites it

219 citing papers in PubMed.

  1. Trial
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  8. HIV-1 DNA decay dynamics in blood during more than a decade of suppressive antiretroviral therapy.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2014
    Trial
  9. Trial
  10. Trial
  11. Modelling HIV-1 2-LTR dynamics following raltegravir intensification.Journal of the Royal Society, Interface · 2013
    Trial
  12. Trial
  13. Trial
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  15. Trial
  16. Review
  17. Article
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  19. Article
  20. Article

159 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

18 authors.

Frank MaldarelliHIV Drug Resistance Program, National Cancer Institute, Frederick, Maryland, United States of America. fmalli@mail.nih.gov
Sarah Palmer
Martin S King
Ann Wiegand
Michael A Polis
JoAnn Mican
Joseph A Kovacs
Richard T Davey
Diane Rock-Kress
Robin Dewar
Shuying Liu
Julia A Metcalf
Catherine Rehm
Scott C Brun
George J Hanna
Dale J Kempf
John M Coffin
John W Mellors

Funding

Immunologic And Virologic Approaches To HIV-1 TherapeuticsZIAAI000865 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI DAVEY, RICHARD · 2009 to 2019
$8.8M
Immunologic/Virologic Approaches To HIV-1 TherapeuticsZ01AI000865 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI DAVEY, RICHARD · 2000 to 2008
$4.6M
Collaborative Clinical Research Studies of HIV and EmergZ01AI000980 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI POLIS, MICHAEL L. · 2006 to 2006
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6 · The paper itself

Abstract

Current antiretroviral therapy is effective in suppressing but not eliminating HIV-1 infection. Understanding the source of viral persistence is essential for developing strategies to eradicate HIV-1 infection. We therefore investigated the level of plasma HIV-1 RNA in patients with viremia suppressed to less than 50-75 copies/ml on standard protease inhibitor- or non-nucleoside reverse transcriptase inhibitor-containing antiretroviral therapy using a new, real-time PCR-based assay for HIV-1 RNA with a limit of detection of one copy of HIV-1 RNA. Single copy assay results revealed that >80% of patients on initial antiretroviral therapy for 60 wk had persistent viremia of one copy/ml or more with an overall median of 3.1 copies/ml. The level of viremia correlated with pretherapy plasma HIV-1 RNA but not with the specific treatment regimen. Longitudinal studies revealed no significant decline in the level of viremia between 60 and 110 wk of suppressive antiretroviral therapy. These data suggest that the persistent viremia on current antiretroviral therapy is derived, at least in part, from long-lived cells that are infected prior to initiation of therapy.

Indexed as

Anti-HIV AgentsCohort StudiesDouble-Blind MethodDrug Therapy, CombinationHIV-1HIV InfectionsHumansLamivudineLongitudinal StudiesReproducibility of ResultsReverse Transcriptase Polymerase Chain ReactionRNA, ViralSensitivity and SpecificityStavudineViremiaVirus ReplicationAnti-HIV AgentsLamivudineRNA, ViralStavudine

Identifiers

PMID17411338
PMCPMC1847689

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.