Evidence map›Paper›PMID 23922373›Full record

ArticleThe Journal of infectious diseases2014

HIV type 1 polymerase gene polymorphisms are associated with phenotypic differences in replication capacity and disease progression.

Oon Tek Ng, Oliver Laeyendecker, Andrew D Redd, Supriya Munshaw, Mary K Grabowski, Agnes C Paquet, Mark C Evans, Mojgan Haddad, Wei Huang, Merlin L Robb and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

16 citing papers in PubMed, 20 citations in OpenAlex.

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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

16 authors at 7 institutions in 3 countries.

Oon Tek NgDepartment of Medicine.
Oliver Laeyendecker
Andrew D Redd
Supriya Munshaw
Mary K Grabowski
Agnes C Paquet
Mark C Evans
Mojgan Haddad
Wei Huang
Merlin L Robb
Steven J Reynolds
Ronald H Gray
Maria J Wawer
David Serwadda
Susan H Eshleman
Thomas C Quinn
Ideaya Biosciences (United States) · USJohns Hopkins University · USNational Institute of Allergy and Infectious Diseases · USJackson Foundation · USMakerere University · UGNational Institutes of Health · USTan Tock Seng Hospital · SG

Funding

LC: HIV Prevention Trials Network - Laboratory Support for the SARS-CoV-2 Seroprevalence Study (CoVPN 5002)UM1AI068613 · NIAID · JOHNS HOPKINS UNIVERSITY · PI SUSAN H ESHLEMAN, Mark A Marzinke · 2011 to 2026
$100.2M
International Center for Excellence in Research (ICER) in Uganda: Impact of ARVsZIAAI001040 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI REYNOLDS, STEVEN · 2009 to 2025
$23.5M
HIV Prevention Trials Network: Network LaboratoryU01AI068613 · NIAID · JOHNS HOPKINS UNIVERSITY · PI ESHLEMAN, SUSAN H · 2006 to 2010
$16.5M
International Studies of the Acquired Immune Deficiency Syndrome (AIDS)ZIAAI000361 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI REDD, ANDREW · 2009 to 2025
$15.8M
Mechanisms of Hepatitis C Virus EvolutionR01DA024565 · NIDA · JOHNS HOPKINS UNIVERSITY · PI RAY, STUART C · 2007 to 2011
$2.6M
Intramural NIH HHSNIAID NIH HHS UM1 AI068613NIDA NIH HHS R01 DA024565
6 · The paper itself

Abstract

backgroundDeterminants of intersubtype differences in human immunodeficiency virus type 1 (HIV-1) clinical disease progression remain unknown.

methodsHIV-1 subtype was independently determined for 5 separate genomic regions in 396 HIV-1 seroconverters from Rakai, Uganda, using a multiregion hybridization assay. Replication capacities (RC) in samples from a subset of 145 of these subjects were determined. HIV-1 genomic regions and pol RC were examined for association with disease progression. Amino acid polymorphisms were examined for association with pol RC.

resultsIn multivariate analyses, the hazard for progression to the composite end point (defined as a CD4(+) T-cell count <250 cells/mm(3), antiretroviral therapy initiation, or death) among patients with subtype D pol infection was 2.4 times the hazard for those infected with subtype A pol infection (P = .001). Compared with subtype A pol (the reference group), the hazard for progression to the composite end point for subtype D pol infection with a pol RC >67% (ie, the median pol RC) was significantly greater (HR, 4.6; 95% confidence interval [CI], 1.9-11.0; P = .001), whereas the hazard for progression to the composite end point for subtype D pol infection with a pol RC ≤67% was not significantly different (HR, 2.2; 95% CI, 1.0-4.9; P = .051). Amino acid substitutions at protease positions 62 and 64 and at reverse transcriptase position 272 were associated with significant differences in pol RC.

conclusionsHIV-1 pol gene intersubtype and RC differences are associated with disease progression and may be influenced by amino acid polymorphisms.

Indexed as

Genes, polAdolescentAdultAmino Acid SubstitutionDisease ProgressionFemaleHIV-1HIV InfectionsHumansMaleMiddle AgedPhenotypeUgandaViral LoadVirus Replicationamino acid polymorphismsdisease progressionHIV-1 Subtypepolymerasereplication capacitysubtype Asubtype D

Identifiers

PMID23922373
PMCPMC3864385
OpenAlexW2150861593

What OpenQuestion holds

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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.