Evidence map›Paper›PMID 26334101›Full record

ArticleOncotarget2015

Molecular dissection of HBV evasion from restriction factor tetherin: A new perspective for antiviral cell therapy.

Kei Miyakawa, Satoko Matsunaga, Koichi Watashi, Masaya Sugiyama, Hirokazu Kimura, Naoki Yamamoto, Masashi Mizokami, Takaji Wakita, Akihide Ryo

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 35 citations in OpenAlex.

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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

9 authors at 4 institutions in 2 countries.

Kei MiyakawaDepartment of Microbiology, Yokohama City University School of Medicine, Kanagawa 236-0004, Japan.
Satoko MatsunagaDepartment of Microbiology, Yokohama City University School of Medicine, Kanagawa 236-0004, Japan.
Koichi WatashiDepartment of Virology II, National Institute of Infectious Diseases, Tokyo 162-8640, Japan.
Masaya SugiyamaDepartment of Hepatic Diseases, The Research Center for Hepatitis and Immunology, National Center for Global Health and Medicine, Chiba 272-8516, Japan.
Hirokazu KimuraInfectious Disease Surveillance Center, National Institute of Infectious Diseases, Tokyo 208-0011, Japan.
Naoki YamamotoDepartment of Microbiology, National University of Singapore, Singapore 117597, Singapore.
Masashi MizokamiDepartment of Hepatic Diseases, The Research 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.
National Institute of Infectious Diseases · JPYokohama City University · JPNational Center for Global Health and Medicine · JPNational University of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Viruses have evolved various strategies to escape from the innate cellular mechanisms inhibiting viral replication and spread. Extensive evidence has highlighted the ineffectiveness of interferon (IFN) therapy against chronic hepatitis B virus (HBV) infection, implying the existence of mechanisms by which HBV evades IFN-induced antiviral responses. In our current study, we demonstrate that HBV surface protein (HBs) plays a crucial role in counteracting the IFN-induced antiviral response mediated by tetherin (also known as BST-2). The type I IFN treatment of HBV-producing cells marginally but significantly inhibited the release of HBsAg and viral DNA, but this release was recovered by the knockdown of tetherin. HBs can interact with tetherin via its fourth transmembrane domain thereby inhibiting its dimerization and antiviral activity. The expression of a tetherin mutant devoid of the HBs-binding domain promoted a prominent restriction of HBV particle production that eventually resulted in the alleviation of caspase-1-mediated cytotoxicity and interleukin-1β secretion in induced pluripotent stem cell (iPSC)-derived hepatocytes. Our current results thus reveal a previously undescribed molecular link between HBV and tetherin during the course of an IFN-induced antiviral response. In addition, strategies to augment the antiviral activity of tetherin by impeding tetherin-HBs interactions may be viable as a therapeutic intervention against HBV.

Indexed as

Antigens, CDAntiviral AgentsBone Marrow Stromal Antigen 2GPI-Linked ProteinsHEK293 CellsHepatitis B, ChronicHepatitis B Surface AntigensHepatitis B virusHepatocytesHep G2 CellsHumansInterferon Type IAntigens, CDAntiviral AgentsBone Marrow Stromal Antigen 2BST2 protein, humanGPI-Linked ProteinsHepatitis B Surface AntigensInterferon Type Ihepatic injuryImmune responseImmunityImmunology and Microbiology Sectionpyroptosis

Identifiers

PMID26334101
PMCPMC4673130
OpenAlexW2096044710

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.