Evidence map›Paper›PMID 19913270›Full record

ArticleVirology2010

Adaptive changes in HIV-1 subtype C proteins during early infection are driven by changes in HLA-associated immune pressure.

F K Treurnicht, C Seoighe, D P Martin, N Wood, M-R Abrahams, D de Assis Rosa, H Bredell, Z Woodman, W Hide, K Mlisana and 3 more

Open access · greenAbstract read
In one paragraph

Article in Virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Addressing an HIV cure in LMIC.Retrovirology · 2021
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Human immunodeficiency virus vaccine trials.Cold Spring Harbor perspectives in medicine · 2012
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Conflicting selection pressures on T-cell epitopes in HIV-1 subtype B.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2011
    Article
  18. Article
  19. Review
  20. Article
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

13 authors at 4 institutions in 1 country.

F K TreurnichtInstitute of Infectious Diseases and Molecular Medicine (IIDMM), Division of Medical Virology, University of Cape Town, South Africa.
C Seoighe
D P Martin
N Wood
M-R Abrahams
D de Assis Rosa
H Bredell
Z Woodman
W Hide
K Mlisana
S Abdool Karim
C M Gray
C Williamson
University of Cape Town · ZACentre for the AIDS Programme of Research in South Africa · ZARespiratory and Meningeal Pathogens Research Unit · ZAUniversity of the Western Cape · ZA

Funding

The Viral Set Point in HIV-1 Subtype C InfectionU19AI051794 · NIAID · UNIVERSITY OF KWAZULU-NATAL · PI ABDOOL KARIM, SALIM S · 2002 to 2007
$22.5M
NIAID NIH HHS AI51794NIAID NIH HHS U19 AI051794Wellcome Trust
6 · The paper itself

Abstract

It is unresolved whether recently transmitted human immunodeficiency viruses (HIV) have genetic features that specifically favour their transmissibility. To identify potential "transmission signatures", we compared 20 full-length HIV-1 subtype C genomes from primary infections, with 66 sampled from ethnically and geographically matched individuals with chronic infections. Controlling for recombination and phylogenetic relatedness, we identified 39 sites at which amino acid frequency spectra differed significantly between groups. These sites were predominantly located within Env, Pol and Gag (14/39, 9/39 and 6/39 respectively) and were significantly clustered (33/39) within known immunoreactive peptides. Within 6 months of infection, we detected reversion-to-consensus mutations at 14 sites and potential CTL escape mutations at seven. Here we provide evidence that frequent reversion mutations probably allows the virus to recover replicative fitness which, together with immune escape driven by the HLA alleles of the new hosts, differentiate sequences from chronic infections from those sampled shortly after transmission.

Indexed as

Amino Acid SubstitutionDisease ProgressionFemaleGenome, ViralHIV-1HIV InfectionsHLA AntigensHumansImmune EvasionMolecular Sequence DataMutationSequence AlignmentSequence Analysis, ProteinViral Envelope ProteinsHLA AntigensViral Envelope Proteins

Identifiers

PMID19913270
PMCPMC2810538
OpenAlexW2169616551

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.