Evidence map›Paper›PMID 16188997›Full record

ArticleJournal of virology2005

De novo generation of escape variant-specific CD8+ T-cell responses following cytotoxic T-lymphocyte escape in chronic human immunodeficiency virus type 1 infection.

Todd M Allen, Xu G Yu, Elizabeth T Kalife, Laura L Reyor, Mathias Lichterfeld, Mina John, Michael Cheng, Rachel L Allgaier, Stanley Mui, Nicole Frahm and 8 more

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
5.0field-weighted citation impact, top 3% 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

81 citing papers in PubMed, 135 citations in OpenAlex.

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  16. Review
  17. Article
  18. CD8Viral immunology · 2018
    Article
  19. Role of HIV-specific CD8The Journal of experimental medicine · 2017
    Article
  20. Article

21 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 at 3 institutions in 2 countries.

Todd M AllenPartners AIDS Research Center, Massachusetts General Hospital, Boston, 02129, USA.
Xu G Yu
Elizabeth T Kalife
Laura L Reyor
Mathias Lichterfeld
Mina John
Michael Cheng
Rachel L Allgaier
Stanley Mui
Nicole Frahm
Galit Alter
Nancy V Brown
Mary N Johnston
Eric S Rosenberg
Simon A Mallal
Christian Brander
Bruce D Walker
Marcus Altfeld
Massachusetts General Hospital · USHarvard University · USRoyal Perth Hospital · AU

Funding

PATHOGENESIS AND TREATMENT OF ACUTE HIV INFECTIONU01AI052403 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI WALKER, BRUCE D · 2002 to 2006
$10.5M
CTL Responses to Regulatory and Accessory HIV-1 ProteinsR01AI050429 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI ALTFELD, MARCUS · 2002 to 2011
$3.7M
Acute CTL Escape and Viral Variation in HIVR01AI054178 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI ALLEN, TODD M · 2003 to 2007
$2.1M
HIV-1-SPECIFIC T CELL CLONESR01AI028568 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI WALKER, BRUCE D · 1989 to 2008
$1.9M
HIV-1 SPECIFIC T CELL CLONESR37AI028568 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI WALKER, BRUCE D · 1994 to 2003
$1.6M
Impact of CTL Escape Mutations on HIV-1 Replicative FitnessR56AI054178 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI ALLEN, TODD M · 2009 to 2009
$442k
NIAID NIH HHS AI054178NIAID NIH HHS AI28568NIAID NIH HHS AI50429NIAID NIH HHS R01 AI028568NIAID NIH HHS R01 AI050429NIAID NIH HHS R01 AI054178NIAID NIH HHS R37 AI028568NIAID NIH HHS R56 AI054178NIAID NIH HHS U01 AI052403NIAID NIH HHS U01 AI52403
6 · The paper itself

Abstract

Human immunodeficiency virus type 1 (HIV-1) evades CD8(+) T-cell responses through mutations within targeted epitopes, but little is known regarding its ability to generate de novo CD8(+) T-cell responses to such mutants. Here we examined gamma interferon-positive, HIV-1-specific CD8(+) T-cell responses and autologous viral sequences in an HIV-1-infected individual for more than 6 years following acute infection. Fourteen optimal HIV-1 T-cell epitopes were targeted by CD8(+) T cells, four of which underwent mutation associated with dramatic loss of the original CD8(+) response. However, following the G(357)S escape in the HLA-A11-restricted Gag(349-359) epitope and the decline of wild-type-specific CD8(+) T-cell responses, a novel CD8(+) T-cell response equal in magnitude to the original response was generated against the variant epitope. CD8(+) T cells targeting the variant epitope did not exhibit cross-reactivity against the wild-type epitope but rather utilized a distinct T-cell receptor Vbeta repertoire. Additional studies of chronically HIV-1-infected individuals expressing HLA-A11 demonstrated that the majority of the subjects targeted the G(357)S escape variant of the Gag(349-359) epitope, while the wild-type consensus sequence was significantly less frequently recognized. These data demonstrate that de novo responses against escape variants of CD8(+) T-cell epitopes can be generated in chronic HIV-1 infection and provide the rationale for developing vaccines to induce CD8(+) T-cell responses directed against both the wild-type and variant forms of CD8 epitopes to prevent the emergence of cytotoxic T-lymphocyte escape variants.

Indexed as

CD8-Positive T-LymphocytesChronic DiseaseEpitopes, T-LymphocyteHIV-1HIV Core Protein p24HIV InfectionsHLA-A11 AntigenHLA-A AntigensHumansMolecular Sequence DataMutationReceptors, Antigen, T-Cell, alpha-betaSpecies SpecificityT-Lymphocytes, CytotoxicEpitopes, T-LymphocyteHIV Core Protein p24HLA-A11 AntigenHLA-A AntigensReceptors, Antigen, T-Cell, alpha-beta

Identifiers

PMID16188997
PMCPMC1235830
OpenAlexW2058894986

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.