Evidence map›Paper›PMID 27626689›Full record

ArticleOncotarget2016

Interferon-stimulated gene of 20 kDa protein (ISG20) degrades RNA of hepatitis B virus to impede the replication of HBV in vitro and in vivo.

Chean Ring Leong, Kenji Funami, Hiroyuki Oshiumi, Deng Mengao, Hiromi Takaki, Misako Matsumoto, Hussein H Aly, Koichi Watashi, Kazuaki Chayama, Tsukasa Seya

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

32 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  4. ISG20 RestrictsMicroorganisms · 2025
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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

10 authors at 3 institutions in 2 countries.

Chean Ring LeongDepartment of Microbiology and Immunology, Graduate School of Medicine, Hokkaido University, Sapporo, 060-8638 Japan.
Kenji FunamiDepartment of Microbiology and Immunology, Graduate School of Medicine, Hokkaido University, Sapporo, 060-8638 Japan.
Hiroyuki OshiumiDepartment of Microbiology and Immunology, Graduate School of Medicine, Hokkaido University, Sapporo, 060-8638 Japan.
Deng MengaoDepartment of Microbiology and Immunology, Graduate School of Medicine, Hokkaido University, Sapporo, 060-8638 Japan.
Hiromi TakakiDepartment of Microbiology and Immunology, Graduate School of Medicine, Hokkaido University, Sapporo, 060-8638 Japan.
Misako MatsumotoDepartment of Microbiology and Immunology, Graduate School of Medicine, Hokkaido University, Sapporo, 060-8638 Japan.
Hussein H AlyDepartment of Virology II, National Institute of Infectious Diseases, Tokyo, 162-8640 Japan.
Koichi WatashiDepartment of Virology II, National Institute of Infectious Diseases, Tokyo, 162-8640 Japan.
Kazuaki ChayamaDepartment of Gastroenterology and Metabolism, Applied Life Sciences, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, 734-8553 Japan.
Tsukasa SeyaDepartment of Microbiology and Immunology, Graduate School of Medicine, Hokkaido University, Sapporo, 060-8638 Japan.
Hokkaido University · JPNational Institute of Infectious Diseases · JPHiroshima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis B virus (HBV) barely induces host interferon (IFN)-stimulated genes (ISGs), which allows efficient HBV replication in the immortalized mouse hepatocytes as per human hepatocytes. Here we found that transfection of Isg20 plasmid robustly inhibits the HBV replication in HBV-infected hepatocytes irrespective of IRF3 or IFN promoter activation. Transfection of Isg20 is thus effective to eradicate HBV in the infected hepatocytes. Transfection of HBV genome or ε-stem of HBV pgRNA (active pgRNA moiety) failed to induce Isg20 in the hepatocytes, while control polyI:C (a viral dsRNA analogue mimic) activated MAVS pathway leading to production of type I IFN and then ISGsg20 via the IFN-α/β receptor (IFNAR). Consistently, addition of IFN-α induced Isg20 and partially suppressed HBV replication in hepatocytes. Chasing HBV RNA, DNA and proteins by blotting indicated that ISG20 expression decreased HBV RNA and replicative DNA in HBV-transfected cells, which resulted in low HBs antigen production and virus titer. The exonuclease domains of ISG20 mainly participated in HBV-RNA decay. In vivo hydrodynamic injection, ISG20 was crucial for suppressing HBV replication without degrading host RNA in the liver. Taken together, ISG20 acts as an innate anti-HBV effector that selectively degrades HBV RNA and blocks replication of infectious HBV particles. ISG20 would be a critical effector for ameliorating chronic HBV infection in the IFN therapy.

Indexed as

AnimalsAntiviral AgentsCell LineCell Line, TumorExonucleasesExoribonucleasesGene Expression ProfilingHepatitis B, ChronicHepatitis B virusHepatocytesHep G2 CellsHumansInterferon-alphaLiverMice, Inbred C57BLMice, KnockoutAntiviral AgentsExonucleasesExoribonucleasesInterferon-alphaISG20 protein, humanReceptor, Interferon alpha-betaRNA, Viralgene therapyhepatitis B virus (HBV)interferon (IFN)interferon-stimulated genes (ISGs)ISG20

Identifiers

PMID27626689
PMCPMC5356548
OpenAlexW2516429582

What OpenQuestion holds

Textmetadata
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.