Evidence map›Paper›PMID 27280548›Full record

ArticlePLoS pathogens2016

Sequential Dysfunction and Progressive Depletion of Candida albicans-Specific CD4 T Cell Response in HIV-1 Infection.

Fengliang Liu, Xiuzhen Fan, Sarah Auclair, Monique Ferguson, Jiaren Sun, Lynn Soong, Wei Hou, Robert R Redfield, Deborah L Birx, Silvia Ratto-Kim and 4 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. HCV-specific CD4EBioMedicine · 2026
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  2. Observational
  3. Enrichment ofFrontiers in immunology · 2026
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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

14 authors at 6 institutions in 3 countries.

Fengliang LiuDepartment of Microbiology & Immunology and Sealy Center for Vaccine Development, University of Texas Medical Branch, Galveston, Texas, United States of America.
Xiuzhen FanDepartment of Microbiology & Immunology and Sealy Center for Vaccine Development, University of Texas Medical Branch, Galveston, Texas, United States of America.
Sarah AuclairDepartment of Microbiology & Immunology and Sealy Center for Vaccine Development, University of Texas Medical Branch, Galveston, Texas, United States of America.
Monique FergusonDivision of Infectious Diseases, University of Texas Medical Branch, Galveston, Texas, United States of America.
Jiaren SunDepartment of Microbiology & Immunology and Sealy Center for Vaccine Development, University of Texas Medical Branch, Galveston, Texas, United States of America.
Lynn SoongDepartment of Microbiology & Immunology and Sealy Center for Vaccine Development, University of Texas Medical Branch, Galveston, Texas, United States of America.
Wei HouSchool of Basic Medical Sciences, Wuhan University, Wuhan, Hubei, China.
Robert R RedfieldInstitute of Human Virology and Division of Infectious Diseases, University of Maryland School of Medicine, Baltimore, Maryland, United States of America.
Deborah L BirxU.S. Military HIV Research Program, Water Reed Army Institute of Research, Silver Spring, Maryland, United States of America.
Silvia Ratto-KimU.S. Military HIV Research Program, Henry M. Jackson Foundation, Silver Spring, Maryland, United States of America.
Merlin L RobbU.S. Military HIV Research Program, Henry M. Jackson Foundation, Silver Spring, Maryland, United States of America.
Jerome H KimInternational Vaccine Institute, Seoul, Republic of Korea; U.S. Military HIV Research Program, Water Reed Army Institute of Research, Silver Spring, Maryland, United States of America.
Nelson L MichaelU.S. Military HIV Research Program, Water Reed Army Institute of Research, Silver Spring, Maryland, United States of America.
Haitao HuDepartment of Microbiology & Immunology and Sealy Center for Vaccine Development, University of Texas Medical Branch, Galveston, Texas, United States of America.
The University of Texas Medical Branch at Galveston · USHenry M. Jackson Foundation · USWalter Reed Army Institute of Research · USInternational Vaccine Institute · KRUniversity of Maryland, Baltimore · USWuhan University · CN

Funding

Susceptibility of antigen-specific CD4 T cells to HIV: implications for HIV vacciR21AI110214 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI HU, HAITAO · 2014 to 2015
$403k
NIAID NIH HHS R21 AI110214
6 · The paper itself

Abstract

Loss of immune control over opportunistic infections can occur at different stages of HIV-1 (HIV) disease, among which mucosal candidiasis caused by the fungal pathogen Candida albicans (C. albicans) is one of the early and common manifestations in HIV-infected human subjects. The underlying immunological basis is not well defined. We have previously shown that compared to cytomegalovirus (CMV)-specific CD4 cells, C. albicans-specific CD4 T cells are highly permissive to HIV in vitro. Here, based on an antiretroviral treatment (ART) naïve HIV infection cohort (RV21), we investigated longitudinally the impact of HIV on C. albicans- and CMV-specific CD4 T-cell immunity in vivo. We found a sequential dysfunction and preferential depletion for C. albicans-specific CD4 T cell response during progressive HIV infection. Compared to Th1 (IFN-γ, MIP-1β) functional subsets, the Th17 functional subsets (IL-17, IL-22) of C. albicans-specific CD4 T cells were more permissive to HIV in vitro and impaired earlier in HIV-infected subjects. Infection history analysis showed that C. albicans-specific CD4 T cells were more susceptible to HIV in vivo, harboring modestly but significantly higher levels of HIV DNA, than CMV-specific CD4 T cells. Longitudinal analysis of HIV-infected individuals with ongoing CD4 depletion demonstrated that C. albicans-specific CD4 T-cell response was preferentially and progressively depleted. Taken together, these data suggest a potential mechanism for earlier loss of immune control over mucosal candidiasis in HIV-infected patients and provide new insights into pathogen-specific immune failure in AIDS pathogenesis.

Indexed as

AIDS-Related Opportunistic InfectionsCandida albicansCandidiasisCD4-Positive T-LymphocytesCytomegalovirusFlow CytometryHIV-1HIV InfectionsHumansPolymerase Chain ReactionTranscriptome

Identifiers

PMID27280548
PMCPMC4900544
OpenAlexW2410167871

What OpenQuestion holds

Textmetadata
LicenceCC0
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.