Evidence map›Paper›PMID 35087074›Full record

ArticleNature communications2022

Galectin-9 restricts hepatitis B virus replication via p62/SQSTM1-mediated selective autophagy of viral core proteins.

Kei Miyakawa, Mayuko Nishi, Michinaga Ogawa, Satoko Matsunaga, Masaya Sugiyama, Hironori Nishitsuji, Hirokazu Kimura, Makoto Ohnishi, Koichi Watashi, Kunitada Shimotohno and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
6.3field-weighted citation impact, top 2% 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

50 citing papers in PubMed, 79 citations in OpenAlex.

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  13. Roles of the Keap1/Nrf2 pathway and mitophagy in liver diseases.Journal of Zhejiang University. Science. B · 2025
    Review
  14. Immunometabolic Targets in CD8Liver cancer · 2025
    Review
  15. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 1 country.

Kei MiyakawaDepartment of Microbiology, Yokohama City University School of Medicine, Kanagawa, 236-0004, Japan.
Mayuko NishiDepartment of Microbiology, Yokohama City University School of Medicine, Kanagawa, 236-0004, Japan.
Michinaga OgawaDepartment of Bacteriology I, National Institute of Infectious Diseases, Tokyo, 162-8640, Japan.ORCID http://orcid.org/0000-0001-6883-6443
Satoko MatsunagaDepartment of Microbiology, Yokohama City University School of Medicine, Kanagawa, 236-0004, Japan.
Masaya SugiyamaGenome Medical Sciences Project, National Center for Global Health and Medicine, Chiba, 272-8516, Japan.
Hironori NishitsujiResearch Center for Hepatitis and Immunology, National Center for Global Health and Medicine, Chiba, 272-8516, Japan.
Hirokazu KimuraSchool of Medical Technology, Faculty of Health Sciences, Gunma Paz University, Gunma, 370-0006, Japan.
Makoto OhnishiDepartment of Bacteriology I, National Institute of Infectious Diseases, Tokyo, 162-8640, Japan.
Koichi WatashiDepartment of Virology II, National Institute of Infectious Diseases, Tokyo, 162-8640, Japan.
Kunitada ShimotohnoResearch Center for Hepatitis and Immunology, National Center for Global Health and Medicine, Chiba, 272-8516, Japan.
Takaji WakitaDepartment of Virology II, National Institute of Infectious Diseases, Tokyo, 162-8640, Japan.
Akihide RyoDepartment of Microbiology, Yokohama City University School of Medicine, Kanagawa, 236-0004, Japan. aryo@yokohama-cu.ac.jp.ORCID http://orcid.org/0000-0001-6028-8091
National Institute of Infectious Diseases · JPYokohama City University · JPNational Center for Global Health and Medicine · JPGumma Paz College · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy has been linked to a wide range of functions, including a degradative process that defends host cells against pathogens. Although the involvement of autophagy in HBV infection has become apparent, it remains unknown whether selective autophagy plays a critical role in HBV restriction. Here, we report that a member of the galectin family, GAL9, directs the autophagic degradation of HBV HBc. BRET screening revealed that GAL9 interacts with HBc in living cells. Ectopic expression of GAL9 induces the formation of HBc-containing cytoplasmic puncta through interaction with another antiviral factor viperin, which co-localized with the autophagosome marker LC3. Mechanistically, GAL9 associates with HBc via viperin at the cytoplasmic puncta and enhanced the auto-ubiquitination of RNF13, resulting in p62 recruitment to form LC3-positive autophagosomes. Notably, both GAL9 and viperin are type I IFN-stimulated genes that act synergistically for the IFN-dependent proteolysis of HBc in HBV-infected hepatocytes. Collectively, these results reveal a previously undescribed antiviral mechanism against HBV in infected cells and a form of crosstalk between the innate immune system and selective autophagy in viral infection.

Indexed as

Antiviral AgentsAutophagosomesAutophagyGalectinsGene ExpressionHEK293 CellsHepatitis BHepatitis B virusHep G2 CellsHumansMacroautophagyProteolysisSequestosome-1 ProteinViral Core ProteinsVirus ReplicationAntiviral AgentsGalectinsLGALS9 protein, humanSequestosome-1 ProteinSQSTM1 protein, humanViral Core Proteins

Identifiers

PMID35087074
PMCPMC8795376
OpenAlexW4210583669

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.