Evidence map›Paper›PMID 27570484›Full record

ArticleInternational journal of biological sciences2016

An Effective Molecular Target Site in Hepatitis B Virus S Gene for Cas9 Cleavage and Mutational Inactivation.

Hao Li, Chunyu Sheng, Hongbo Liu, Guangze Liu, Xinying Du, Juan Du, Linsheng Zhan, Peng Li, Chaojie Yang, Lihua Qi and 14 more

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.3field-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

22 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Frontiers in microbiology · 2022
    Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. CRISPR/Cas technology as a promising weapon to combat viral infections.BioEssays : news and reviews in molecular, cellular and developmental biology · 2021
    Review
  15. CRISPR-Cas9 gene editing of hepatitis B virus in chronically infected humanized mice.Molecular therapy. Methods & clinical development · 2021
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Removal of Integrated Hepatitis B Virus DNA Using CRISPR-Cas9.Frontiers in cellular and infection microbiology · 2017
    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

24 authors at 4 institutions in 3 countries.

Hao LiInstitute of Disease Control and Prevention, Academy of Military Medical Sciences, Beijing, China.
Chunyu ShengInstitute of Disease Control and Prevention, Academy of Military Medical Sciences, Beijing, China.
Hongbo LiuInstitute of Disease Control and Prevention, Academy of Military Medical Sciences, Beijing, China.
Guangze LiuTransgenic Engineering Research Laboratory, Infectious Disease Center, Guangzhou 458 th Hospital, Guangzhou, China.
Xinying DuInstitute of Disease Control and Prevention, Academy of Military Medical Sciences, Beijing, China.
Juan DuLab of Blood-Borne Viruses, Beijing Institute of Transfusion Medicine, Beijing, China.
Linsheng ZhanLab of Blood-Borne Viruses, Beijing Institute of Transfusion Medicine, Beijing, China.
Peng LiInstitute of Disease Control and Prevention, Academy of Military Medical Sciences, Beijing, China.
Chaojie YangInstitute of Disease Control and Prevention, Academy of Military Medical Sciences, Beijing, China.
Lihua QiInstitute of Disease Control and Prevention, Academy of Military Medical Sciences, Beijing, China.
Jian WangInstitute of Disease Control and Prevention, Academy of Military Medical Sciences, Beijing, China.
Xiaoxia YangInstitute of Disease Control and Prevention, Academy of Military Medical Sciences, Beijing, China.
Leili JiaInstitute of Disease Control and Prevention, Academy of Military Medical Sciences, Beijing, China.
Jing XieInstitute of Disease Control and Prevention, Academy of Military Medical Sciences, Beijing, China.
Ligui WangInstitute of Disease Control and Prevention, Academy of Military Medical Sciences, Beijing, China.
Rongzhang HaoInstitute of Disease Control and Prevention, Academy of Military Medical Sciences, Beijing, China.
Dongping XuResearch Center for Liver Failure, Beijing 302 nd Hospital, Beijing, China.
Yigang TongState Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, China.
Yusen ZhouState Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, China.
Jianjun ZhouGladcan Consulting Company, Beijing, China.
Yansong SunInstitute of Disease Control and Prevention, Academy of Military Medical Sciences, Beijing, China.
Qiao LiDepartment of Surgery, University of Michigan, Ann Arbor, MI 48109, USA.
Shaofu QiuInstitute of Disease Control and Prevention, Academy of Military Medical Sciences, Beijing, China.
Hongbin SongInstitute of Disease Control and Prevention, Academy of Military Medical Sciences, Beijing, China.
Academy of Military Medical Sciences · CNGuangzhou Blood Center · CNInstitute of Microbiology · BYUniversity of Michigan–Ann Arbor · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic hepatitis B infection remains incurable because HBV cccDNA can persist indefinitely in patients recovering from acute HBV infection. Given the incidence of HBV infection and the shortcomings of current therapeutic options, a novel antiviral strategy is urgently needed. To inactivate HBV replication and destroy the HBV genome, we employed genome editing tool CRISPR/Cas9. Specifically, we found a CRISPR/Cas9 system (gRNA-S4) that effectively targeted the HBsAg region and could suppress efficiently viral replication with minimal off-target effects and impact on cell viability. The mutation mediated by CRISPR/Cas9 in HBV DNA both in a stable HBV-producing cell line and in HBV transgenic mice had been confirmed and evaluated using deep sequencing. In addition, we demonstrated the reduction of HBV replication was caused by the mutation of S4 site through three S4 region-mutated monoclonal cells. Besides, the gRNA-S4 system could also reduce serum surface-antigen levels by 99.91 ± 0.05% and lowered serum HBV DNA level below the negative threshold in the HBV hydrodynamics mouse model. Together, these findings indicate that the S4 region may be an ideal target for the development of innovative therapies against HBV infection using CRISPR/Cas9.

Indexed as

Antiviral AgentsCRISPR-Cas SystemsHepatitis B virusMutationViral ProteinsVirus ReplicationAntiviral AgentsViral ProteinsCRISPR/Cas9HBV infection

Identifiers

PMID27570484
PMCPMC4997054
OpenAlexW2510249192

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.