Evidence map›Paper›PMID 41263016›Full record

ArticleJournal of innate immunity2026

Chloroquine Enhances Mitochondrial Antiviral Signaling-Mediated Cytokine Induction and Alters Mitochondrial Morphology.

Yu-Ting Kao, Wei-Sheng Chen, Chi-Ting Shie, Chia-Yi Yu

Abstract read
In one paragraph

Article in Journal of innate immunity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

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4 · The record

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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

4 authors.

Yu-Ting KaoM.Sc. Program in Tropical Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan, yutingkao@kmu.edu.tw.
Wei-Sheng ChenDepartment of Microbiology and Immunology, National Cheng Kung University, Tainan, Taiwan.
Chi-Ting ShieNational Institute of Infectious Diseases and Vaccinology, National Health Research Institutes, Miaoli, Taiwan.
Chia-Yi YuDepartment of Microbiology and Immunology, National Cheng Kung University, Tainan, Taiwan, epitope@nhri.org.tw.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionChloroquine (CQ), a well-known antimalarial agent, has been proposed as a potential antiviral compound due to its ability to interfere with multiple cellular pathways critical for viral replication. Although CQ exhibits broad-spectrum antiviral activity, its effect on host innate immune responses remains incompletely understood. The timing of CQ administration, whether before or after infection, may lead to different immunological outcomes. Therefore, the immunomodulatory effects of CQ should be carefully evaluated before antiviral therapy.

methodsTo investigate the immunomodulatory role of CQ (50 μ<sc>m</sc>), we used immunofluorescence staining, Western blotting, and reporter assays to evaluate innate immune activation in A549 cells. We established a doxycycline-inducible system to activate mitochondrial antiviral signaling (MAVS)-mediated signaling without viral infection. Plaque assays and antiviral tests were performed to measure viral replication, while cytokine array and RT-qPCR were used to quantify cytokine production. Mitochondrial morphology was assessed using immunofluorescence microscopy.

resultsCQ enhanced innate immune responses triggered by dengue virus infection and poly(I:C) stimulation. This enhancement was associated with the activation of the MAVS protein and its upstream receptors, including retinoic acid-inducible gene I and melanoma differentiation-associated protein 5. CQ strengthened MAVS-dependent antiviral signaling and increased IL-6 induction more than 13-fold. Alterations in mitochondrial morphology may contribute to this immunostimulatory effect.

conclusionCQ promotes MAVS-mediated antiviral and inflammatory cytokine responses, potentially through its effect on mitochondrial dynamics. These findings indicate that while CQ may enhance antiviral defense, its immune-stimulating properties should be carefully evaluated prior to its use as an antiviral agent in treating RNA virus infections.

Indexed as

Antiviral AgentsChloroquineMitochondriaA549 CellsAdaptor Proteins, Signal TransducingCytokinesHumansImmunity, InnatePoly I-CSignal TransductionVirus ReplicationAdaptor Proteins, Signal TransducingAntiviral AgentsChloroquineCytokinesMAVS protein, humanPoly I-CChloroquineCytokinesInterferonMitochondriaMitochondrial antiviral signaling

Identifiers

PMID41263016
PMCPMC12726877

What Socratic holds

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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 Socratic graph.