Evidence map›Paper›PMID 19116249›Full record

ArticleJournal of virology2009

Human immunodeficiency virus type 1 population genetics and adaptation in newly infected individuals.

M Kearney, F Maldarelli, W Shao, J B Margolick, E S Daar, J W Mellors, V Rao, J M Coffin, S Palmer

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers.

0numbers the graph read from it
0cells of the map it votes in
122citing papers in PubMed
4.5field-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

122 citing papers in PubMed, 167 citations in OpenAlex.

  1. Trial
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  3. Broad activation of latent HIV-1 in vivo.Nature communications · 2016
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  17. Addressing an HIV cure in LMIC.Retrovirology · 2021
    Review
  18. Article
  19. Article
  20. Article

62 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

9 authors at 7 institutions in 1 country.

M KearneyHIV Drug Resistance Program, National Cancer Institute at Frederick, 1050 Boyles Street, Building 535, Room 109, Frederick, MD 21702-1201, USA. kearneym@ncifcrf.gov
F Maldarelli
W Shao
J B Margolick
E S Daar
J W Mellors
V Rao
J M Coffin
S Palmer
National Institutes of Health · USJohns Hopkins University · USScience Applications International Corporation (United States) · USThe Lundquist Institute · USTufts University · USUniversity of America · USUniversity of Pittsburgh · US

Funding

Southern California Primary Infection ProgramU01AI043638 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RICHMAN, DOUGLAS D · 1998 to 2010
$21.3M
HIV-1 Genetic Variation in Infected IndividualsZIABC010819 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI MALDARELLI, FRANK · 2009 to 2025
$9.9M
ACUTE INFECTION AND EARLY DISEASE RESEARCH NETWORKU01AI041532 · NIAID · JOHNS HOPKINS UNIVERSITY · PI MARGOLICK, JOSEPH B. · 1997 to 2003
$3.3M
HIV-1 Genetic Variation in Infected IndividualsZ01BC010819 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI MALDARELLI, FRANK · 2007 to 2008
$1.1M
Intramural NIH HHS Z01 BC010819NCRR NIH HHS M01-RR004425NIAID NIH HHS AI043638NIAID NIH HHS AI 41532NIAID NIH HHS U01 AI041532NIAID NIH HHS U01 AI043638
6 · The paper itself

Abstract

Studies on human immunodeficiency virus type 1 (HIV-1) diversity are critical for understanding viral pathogenesis and the emergence of immune escape variants and for design of vaccine strategies. To investigate HIV-1 population genetics, we used single-genome sequencing to obtain pro-pol and env sequences from longitudinal samples (n = 93) from 14 acutely or recently infected patients. The first available sample after infection for 12/14 patients revealed HIV-1 populations with low genetic diversity, consistent with transmission or outgrowth of a single variant. In contrast, two patients showed high diversity and coexistence of distinct virus populations in samples collected days after a nonreactive enzyme-linked immunosorbent assay or indeterminate Western blot, consistent with transmission or outgrowth of multiple variants. Comparison of PR and RT sequences from the first sample for all patients with the consensus subgroup B sequence revealed that nearly all nonsynonymous differences were confined to identified cytotoxic T-lymphocyte (CTL) epitopes. For HLA-typed patients, mutations compared to the consensus in transmitted variants were found in epitopes that would not be recognized by the patient's major histocompatibility complex type. Reversion of transmitted mutations was rarely seen over the study interval (up to 5 years). These data indicate that acute subtype B HIV-1 infection usually results from transmission or outgrowth of single viral variants carrying mutations in CTL epitopes that were selected prior to transmission either in the donor or in a previous donor and that reversion of these mutations can be very slow. These results have important implications for vaccine strategies because they imply that some HLA alleles could be compromised in newly acquired HIV infections.

Indexed as

Polymorphism, GeneticAdultAmino Acid SubstitutionEpitopes, T-LymphocyteEvolution, MolecularFemaleHIV-1HIV InfectionsHIV ProteaseHIV Reverse TranscriptaseHumansLongitudinal StudiesMaleMiddle AgedMutation, MissenseSequence Analysis, DNAEpitopes, T-LymphocyteHIV ProteaseHIV Reverse Transcriptasep16 protease, Human immunodeficiency virus 1reverse transcriptase, Human immunodeficiency virus 1

Identifiers

PMID19116249
PMCPMC2648286
OpenAlexW2172297142

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.