Evidence map›Paper›PMID 31398241›Full record

ArticlePLoS pathogens2019

CD8 T cells targeting adapted epitopes in chronic HIV infection promote dendritic cell maturation and CD4 T cell trans-infection.

Kai Qin, Sushma Boppana, Victor Y Du, Jonathan M Carlson, Ling Yue, Dario A Dilernia, Eric Hunter, Robbie B Mailliard, Simon A Mallal, Anju Bansal and 1 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Functional Profile of CD8Frontiers in immunology · 2022
    Article
  4. Article
  5. Article
  6. Article
  7. Article
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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

11 authors at 6 institutions in 1 country.

Kai QinDepartment of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.ORCID 0000-0003-1721-6054
Sushma BoppanaDepartment of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.ORCID 0000-0003-1525-0523
Victor Y DuThe Salk Institute for Biological Studies, La Jolla, California, United States of America.
Jonathan M CarlsonMicrosoft Research, Redmond, Washington, United States of America.ORCID 0000-0001-6618-3653
Ling YueEmory Vaccine Center at Yerkes National Primate Research Center and Department of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia, United States of America.
Dario A DilerniaEmory Vaccine Center at Yerkes National Primate Research Center and Department of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia, United States of America.
Eric HunterEmory Vaccine Center at Yerkes National Primate Research Center and Department of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia, United States of America.ORCID 0000-0002-4273-8631
Robbie B MailliardDepartment of Infectious Diseases and Microbiology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.ORCID 0000-0001-5501-503X
Simon A MallalDivision of Infectious Diseases, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America.
Anju BansalDepartment of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.ORCID 0000-0002-8142-0386
Paul A GoepfertDepartment of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.ORCID 0000-0001-8441-5737
University of Alabama at Birmingham · USEmory University · USMicrosoft (United States) · USSalk Institute for Biological Studies · USUniversity of Pittsburgh · USVanderbilt University Medical Center · US

Funding

Yerkes National Primate Research Center Role of type-I IFN in regulating COVID-19 induced inflammation and pathogenesisP51OD011132 · OD · EMORY UNIVERSITY · PI Joon Sup Lee · 2012 to 2026
$167.0M
XRAY CRYSTALLOGRAPHYP30CA013148 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Robert S Welner · 1985 to 2026
$165.9M
Unsolicited R24 for the CFAR-Network of Integrated Clinical Sciences, CNICSR24AI067039 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Michael S. Saag · 2006 to 2026
$99.4M
Virology CoreP30AI027767 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI OLAF KUTSCH · 1988 to 2026
$84.1M
Tennessee CFAR: Implementation of Culturally Responsive Trauma-Informed Care with Youth with HIV in Memphis, TNP30AI110527 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI John Koethe · 2015 to 2026
$27.5M
CTL and HIV Polymorphisms in Heterosexual TransmissionR01AI064060 · NIAID · EMORY UNIVERSITY · PI GOEPFERT, PAUL A., HUNTER, ERIC · 2005 to 2019
$21.7M
IMMUNOLOGIC DISEASES AND BASIC IMMUNOLOGYT32AI007051 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Laurie Ellen Harrington · 1985 to 2026
$13.1M
ROS Modulation of Innate and Adaptive Immunity in RAP30AR048311 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MOUNTZ, JOHN D · 2001 to 2017
$9.5M
A Rational Approach for HIV Vaccine T Cell Epitope SelectionR01AI112566 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GOEPFERT, PAUL A. · 2014 to 2017
$1.9M
NCI NIH HHS P30 CA013148NIAID NIH HHS P30 AI027767NIAID NIH HHS P30 AI110527NIAID NIH HHS R01 AI064060NIAID NIH HHS R01 AI112566NIAID NIH HHS R24 AI067039NIAID NIH HHS T32 AI007051NIAMS NIH HHS P30 AR048311NIH HHS P51 OD011132
6 · The paper itself

Abstract

HIV-1 frequently escapes from CD8 T cell responses via HLA-I restricted adaptation, leading to the accumulation of adapted epitopes (AE). We previously demonstrated that AE compromise CD8 T cell responses during acute infection and are associated with poor clinical outcomes. Here, we examined the impact of AE on CD8 T cell responses and their biological relevance in chronic HIV infection (CHI). In contrast to acute infection, the majority of AE are immunogenic in CHI. Longitudinal analyses from acute to CHI showed an increased frequency and magnitude of AE-specific IFNγ responses compared to NAE-specific ones. These AE-specific CD8 T cells also were more cytotoxic to CD4 T cells. In addition, AE-specific CD8 T cells expressed lower levels of PD1 and CD57, as well as higher levels of CD28, suggesting a more activated and less exhausted phenotype. During CHI, viral sequencing identified AE-encoding strains as the dominant quasispecies. Despite increased CD4 T cell cytotoxicity, CD8 T cells responding to AE promoted dendritic cell (DC) maturation and CD4 T cell trans-infection perhaps explaining why AE are predominant in CHI. Taken together, our data suggests that the emergence of AE-specific CD8 T cell responses in CHI confers a selective advantage to the virus by promoting DC-mediated CD4 T cell trans-infection.

Indexed as

CD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCross-Sectional StudiesDendritic CellsEpitopes, T-LymphocyteFemaleHIV-1HIV InfectionsHumansInterferon-gammaLongitudinal StudiesMaleT-Lymphocytes, CytotoxicViral LoadEpitopes, T-LymphocyteInterferon-gamma

Identifiers

PMID31398241
PMCPMC6703693
OpenAlexW2967745827

What OpenQuestion holds

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LicenceCC BY
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.