Evidence map›Paper›PMID 40872811›Full record

ArticleViruses2025

Persistent Type I Interferon Signaling Impairs Innate Lymphoid Cells During HIV-1 Infection Under Suppressive ART.

Runpeng Han, Haisheng Yu, Guangming Li, Lishan Su, Liang Cheng

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Viruses, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Targeting the pDC/IFN-I axis in HIV-1 immunotherapy.Current opinion in HIV and AIDS · 2026
    Review
  2. Review
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

5 authors.

Runpeng HanState Key Laboratory of Virology and Biosafety, Department of Infectious Diseases, Medical Research Institute, Frontier Science Center for Immunology and Metabolism, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan 430071, China.ORCID 0000-0002-4646-6928
Haisheng YuLineberger Comprehensive Cancer Center, Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.ORCID 0000-0002-1757-1411
Guangming LiLineberger Comprehensive Cancer Center, Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Lishan SuLineberger Comprehensive Cancer Center, Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.ORCID 0000-0002-0350-5560
Liang ChengState Key Laboratory of Virology and Biosafety, Department of Infectious Diseases, Medical Research Institute, Frontier Science Center for Immunology and Metabolism, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan 430071, China.

Funding

Blocking type I interferon signaling to reverse T cell exhaustion and control HIV-1 reservoirsR01AI136990 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI AMARA, RAMA RAO, BOSINGER, STEVEN EDWARD · 2018 to 2022
$4.2M
Immune Mechanisms of Elevated Liver Diseases During HIV InfectionR01DK119937 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SU, LISHAN · 2018 to 2022
$1.9M
Fundamental Research Funds for the Central Universities 2042022dx0003National Key R&D Program 2024YFA1306500National Natural Science Foundation of China 82071784NIAID NIH HHS R01 AI136990NIDDK NIH HHS R01 DK119937NIH HHS 5R01AI136990-06NIH HHS 5R01DK119937-06
6 · The paper itself

Abstract

Persistent type I interferon (IFN-I) signaling compromises adaptive anti-HIV-1 T cell immunity and promotes viral reservoir persistence, yet its effects on innate lymphoid cells during chronic infection remain unclear. Through integrated single-cell RNA sequencing and functional validation in HIV-1-infected humanized mice with combination antiretroviral therapy (cART) and IFN-I signaling blockade, we reveal IFN-I-induced dysfunction of natural killer (NK) cells and group 3 innate lymphoid cells (ILC3s). Mechanistically, the IFN-I-CD9 axis drives NK cells toward a decidual NK cell-like phenotype, impairing their cytotoxic activity. Furthermore, IFNAR blockade rescues ILC3 functionality, which is critical for IL-17/IL-22-mediated antimicrobial defense and mucosal barrier maintenance. Our study delineates IFN-I-driven immunosuppression across innate lymphocyte compartments and proposes the targeted modulation of this pathway to enhance antiviral and mucosal immunity in HIV-1 management.

Indexed as

Anti-Retroviral AgentsHIV-1HIV InfectionsImmunity, InnateInterferon Type ILymphocytesSignal TransductionAnimalsFemaleHumansKiller Cells, NaturalMiceAnti-Retroviral AgentsInterferon Type Ihuman immunodeficiency virushumanized miceimmunopathogenesisinnate lymphoid cellstype-I interferon

Identifiers

PMID40872811
PMCPMC12390710

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.