Evidence map›Paper›PMID 42304389›Full record

ArticleJournal of translational medicine2026

The mitochondrial GTPase ERAL1 inhibits HBV replication by triggering the MAVS signaling cascade.

Caorui Lin, Xiaosang Zheng, Kaixin Chen, Ning Ran, Linjie Luo, Xin Zhang, Ying Huang, Jiawei Zhang, Hanyong Zhu, Jieying He and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

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

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Caorui Lin *Department of Laboratory Medicine, Fujian Key Laboratory of Laboratory Medicine, Fujian Clinical Research Center for Laboratory Medicine of Immunology, Gene Diagnosis Research Center, National Reginal Medical Center, Binhai Campus of the First Affiliated Hospital, The First Affiliated Hospital, Fujian Medical University, Fuzhou, Fujian, China.ORCID 0000-0002-8680-3159
Xiaosang Zheng *Department of Laboratory Medicine, Fujian Key Laboratory of Laboratory Medicine, Fujian Clinical Research Center for Laboratory Medicine of Immunology, Gene Diagnosis Research Center, National Reginal Medical Center, Binhai Campus of the First Affiliated Hospital, The First Affiliated Hospital, Fujian Medical University, Fuzhou, Fujian, China.
Kaixin ChenDepartment of Laboratory Medicine, Fujian Key Laboratory of Laboratory Medicine, Fujian Clinical Research Center for Laboratory Medicine of Immunology, Gene Diagnosis Research Center, National Reginal Medical Center, Binhai Campus of the First Affiliated Hospital, The First Affiliated Hospital, Fujian Medical University, Fuzhou, Fujian, China.
Ning RanInstitute of Medical Sciences, The Second Qilu Hospital & Orthopedic Research Center of Shandong University, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.
Linjie LuoDepartment of Laboratory Medicine, Fujian Key Laboratory of Laboratory Medicine, Fujian Clinical Research Center for Laboratory Medicine of Immunology, Gene Diagnosis Research Center, National Reginal Medical Center, Binhai Campus of the First Affiliated Hospital, The First Affiliated Hospital, Fujian Medical University, Fuzhou, Fujian, China.
Xin ZhangDepartment of Laboratory Medicine, Fujian Key Laboratory of Laboratory Medicine, Fujian Clinical Research Center for Laboratory Medicine of Immunology, Gene Diagnosis Research Center, National Reginal Medical Center, Binhai Campus of the First Affiliated Hospital, The First Affiliated Hospital, Fujian Medical University, Fuzhou, Fujian, China.
Ying HuangDepartment of Laboratory Medicine, Fujian Key Laboratory of Laboratory Medicine, Fujian Clinical Research Center for Laboratory Medicine of Immunology, Gene Diagnosis Research Center, National Reginal Medical Center, Binhai Campus of the First Affiliated Hospital, The First Affiliated Hospital, Fujian Medical University, Fuzhou, Fujian, China.
Jiawei ZhangDepartment of Laboratory Medicine, Fujian Key Laboratory of Laboratory Medicine, Fujian Clinical Research Center for Laboratory Medicine of Immunology, Gene Diagnosis Research Center, National Reginal Medical Center, Binhai Campus of the First Affiliated Hospital, The First Affiliated Hospital, Fujian Medical University, Fuzhou, Fujian, China.
Hanyong ZhuDepartment of Laboratory Medicine, Fujian Key Laboratory of Laboratory Medicine, Fujian Clinical Research Center for Laboratory Medicine of Immunology, Gene Diagnosis Research Center, National Reginal Medical Center, Binhai Campus of the First Affiliated Hospital, The First Affiliated Hospital, Fujian Medical University, Fuzhou, Fujian, China.
Jieying HeDepartment of Laboratory Medicine, Fujian Key Laboratory of Laboratory Medicine, Fujian Clinical Research Center for Laboratory Medicine of Immunology, Gene Diagnosis Research Center, National Reginal Medical Center, Binhai Campus of the First Affiliated Hospital, The First Affiliated Hospital, Fujian Medical University, Fuzhou, Fujian, China.
Bin YangDepartment of Laboratory Medicine, Fujian Key Laboratory of Laboratory Medicine, Fujian Clinical Research Center for Laboratory Medicine of Immunology, Gene Diagnosis Research Center, National Reginal Medical Center, Binhai Campus of the First Affiliated Hospital, The First Affiliated Hospital, Fujian Medical University, Fuzhou, Fujian, China.
Qishui OuDepartment of Laboratory Medicine, Fujian Key Laboratory of Laboratory Medicine, Fujian Clinical Research Center for Laboratory Medicine of Immunology, Gene Diagnosis Research Center, National Reginal Medical Center, Binhai Campus of the First Affiliated Hospital, The First Affiliated Hospital, Fujian Medical University, Fuzhou, Fujian, China. ouqishui@fjmu.edu.cn.
Can LiuDepartment of Laboratory Medicine, Fujian Key Laboratory of Laboratory Medicine, Fujian Clinical Research Center for Laboratory Medicine of Immunology, Gene Diagnosis Research Center, National Reginal Medical Center, Binhai Campus of the First Affiliated Hospital, The First Affiliated Hospital, Fujian Medical University, Fuzhou, Fujian, China. liucan@fjmu.edu.cn.

Funding

China Postdoctoral Science Foundation GZB20240404National Major Science and Technology Projects of China 2026ZD01912700National Natural Science Foundation of China 82372317
6 · The paper itself

Abstract

BACKGROUND AND

aimsMitochondrial GTPase ERA G-protein-like 1 (ERAL1) is considered an antiviral host factor against RNA viruses. However, its role in driving DNA virus infection, particularly hepatitis B virus (HBV) infection, and its relevance to human liver disease are unknown. This study aimed to define the function and molecular mechanism of ERAL1 in HBV pathogenesis.

methodsComplementary models, including HBV-replicating cell lines, an rAAV8-HBV hydrodynamic mouse model, and clinical samples from patients across the natural history of chronic HBV infection were employed and analyzed via coimmunoprecipitation, confocal immunofluorescence, RNA sequencing, qPCR, immunoblotting, and immunohistochemistry.

resultsERAL1 expression was significantly suppressed in HBV patients, including an approximately 75% reduction in the livers of patients during the immune-reactive phase compared with those in healthy controls. ERAL1 overexpression resulted in notable antiviral activity, suppressed HBV replication and achieved nearly 60% HBsAg clearance in vivo. Mechanistically, ERAL1 interacts with mitochondrial adaptor MAVS, promoting its aggregation and subsequently activating the downstream Akt and MAPK signaling pathways, which are essential for its antiviral effect.

conclusionsERAL1 is identified as a crucial HBV-restricting host factor and a novel mitochondria-centered defense mechanism in which ERAL1 reinforces MAVS-dependent antiviral signaling. The notable downregulation of ERAL1 in patient livers and its considerable antiviral effectiveness suggest that ERAL1 is a candidate host factor worthy of further therapeutic exploration.

Indexed as

Adaptor Proteins, Signal TransducingGTP PhosphohydrolasesHepatitis B virusMitochondriaSignal TransductionVirus ReplicationAnimalsFemaleHepatitis BHumansLiverMitochondrial ProteinsProtein BindingAdaptor Proteins, Signal TransducingGTP PhosphohydrolasesMAVS protein, humanMitochondrial ProteinsERA G-protein-like 1Hepatitis B virusMitochondriaMitochondrial antiviral-signaling protein

Identifiers

PMID42304389
PMCPMC13520529

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.