Evidence map›Paper›PMID 24509240›Full record

ArticleAntiviral research2014

Inhibition of hepatitis B virus replication by ligand-mediated activation of RNase L.

Il-Hyun Park, Young-Chan Kwon, Wang-Shick Ryu, Byung-Yoon Ahn

Open access · greenAbstract read
In one paragraph

Article in Antiviral research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. When Hepatitis B Virus Meets Interferons.Frontiers in microbiology · 2018
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Novel fluoronucleoside analog NCC inhibits lamivudine-resistant hepatitis B virus in a hepatocyte model.The Brazilian journal of infectious diseases : an official publication of the Brazilian Society of Infectious Diseases
    Article
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

4 authors at 2 institutions in 1 country.

Il-Hyun ParkDepartment of Life Sciences, Korea University, Anam-dong 5-1, Seoul 136-701, Republic of Korea.
Young-Chan KwonDepartment of Life Sciences, Korea University, Anam-dong 5-1, Seoul 136-701, Republic of Korea.
Wang-Shick RyuDepartment of Biochemistry, Yonsei University, Yonsei-ro 50, Seoul 120-749, Republic of Korea.
Byung-Yoon AhnDepartment of Life Sciences, Korea University, Anam-dong 5-1, Seoul 136-701, Republic of Korea. Electronic address: ahnbyung@korea.ac.kr.
Korea University · KRYonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RNase L is a cellular endoribonuclease that is activated by 2',5'-linked oligoadenylates (2-5A), which are unique and specific ligands synthesized by a family of interferon-inducible, dsRNA-activated enzymes named oligoadenylate synthetases. In the typical antiviral pathway, activated RNase L degrades viral and cellular RNAs, thus limiting viral replication and spread. Although the antiviral activity of RNase L has been demonstrated for several RNA viruses, there is little evidence regarding its role against DNA viruses. In the present study, the potential antiviral activity of RNase L against hepatitis B virus (HBV) was explored utilizing the recently reported infection protocol based on human hepatoma HepG2 cells stably complemented with the virus entry factor NTCP. Viral replication and expression in this cell type was markedly inhibited by poly(I:C)- or 2-5A-mediated activation of RNase L; however, the inhibition was significantly reversed by RNase L knockdown. Further analysis in HBV1.2-transfected Huh-7 hepatoma cells indicated that the antiviral activity of RNase L depends on its ribonuclease function. We also provide evidence for the specific roles of OAS family members in this process. These results suggest that HBV replication can be regulated through interferon-mediated RNA decay pathways and that activation of these host antiviral factors may represent a novel therapeutic strategy for HBV infection.

Indexed as

Virus ReplicationAdenine NucleotidesCell LineEndoribonucleasesEnzyme ActivationGene ExpressionGene Knockdown TechniquesHepatitis B virusHumansIsoenzymesLigandsOligoribonucleotidesPoly I-C2-5A-dependent ribonuclease2',5'-oligoadenylateAdenine NucleotidesEndoribonucleasesIsoenzymesLigandsOligoribonucleotidesPoly I-CHepatitis B virusInterferonOligoadenylate synthetaseRNA decayRNase L

Identifiers

PMID24509240
PMCPMC7119188
OpenAlexW2158324673

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.