Evidence map›Paper›PMID 25652100›Full record

ArticleGene therapy2015

Harnessing the clustered regularly interspaced short palindromic repeat (CRISPR)/CRISPR-associated Cas9 system to disrupt the hepatitis B virus.

S Zhen, L Hua, Y-H Liu, L-C Gao, J Fu, D-Y Wan, L-H Dong, H-F Song, X Gao

Abstract read
PubMed Publisher
In one paragraph

Article in Gene therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
128citing papers in PubMed, 1 pooled it
15.8field-weighted citation impact, top 1% 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

128 citing papers in PubMed, 1 synthesis or guideline pooled it, 232 citations in OpenAlex.

  1. Pooled it
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  9. Towards the elimination of infectious HPV: exploiting CRISPR/Cas innovations.Frontiers in cellular and infection microbiology · 2025
    Review
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  12. Article
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  20. CRISPR-Cas12b enables a highly efficient attack on HIV proviral DNA in T cell cultures.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023
    Article

68 more citing papers are in PubMed but not listed here.

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 1 institution in 2 countries.

S Zhen1] Department of Pharmacology and Toxicology, Beijing Institute of Radiation Medicine, Beijing, China [2] Xijing Hospital, Fourth Military Medical University, Xi'an, China [3] Center for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan.
L Hua1] Department of Pharmacology and Toxicology, Beijing Institute of Radiation Medicine, Beijing, China [2] Laboratory of Pharmacology and Toxicology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, China.
Y-H LiuDepartment of Pharmacology and Toxicology, Beijing Institute of Radiation Medicine, Beijing, China.
L-C GaoDepartment of Pharmacology and Toxicology, Beijing Institute of Radiation Medicine, Beijing, China.
J FuDepartment of Pharmacology and Toxicology, Beijing Institute of Radiation Medicine, Beijing, China.
D-Y WanDepartment of Pharmacology and Toxicology, Beijing Institute of Radiation Medicine, Beijing, China.
L-H DongDepartment of Pharmacology and Toxicology, Beijing Institute of Radiation Medicine, Beijing, China.
H-F SongDepartment of Pharmacology and Toxicology, Beijing Institute of Radiation Medicine, Beijing, China.
X GaoDepartment of Pharmacology and Toxicology, Beijing Institute of Radiation Medicine, Beijing, China.
Beijing Radiation Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The current therapies to treat hepatitis B virus (HBV) infection are limited. Recently, clustered regularly interspaced short palindromic repeat (CRISPR) systems, originally identified in bacteria and archaea, have been found to consist of an RNA-based adaptive immune system that degrades complimentary sequences of invading plasmids and viruses. Here, we studied the effects of the CRISPR/CRISPR-associated Cas9 system that was targeted to the surface antigen (HBsAg)-encoding region of HBV, both in a cell culture system and in vivo. The HBsAg levels in the media of the cells and in the sera of mice were analyzed by a quantitative enzyme-linked immunosorbent assay. The HBV DNA levels were assessed by quantitative PCR and HBsAg expression in mouse livers was assessed by an immunohistochemical assay. The amount of HBsAg secreted in the cell culture and mouse serum was reduced by CRISPR/Cas9 treatment. Immunohistochemistry analyses showed almost no HBsAg-positive cells in the liver tissue of CRISPR/Cas9-S1+X3-treated mice. The CRISPR/Cas9 system efficiently produced mutations in HBV DNA. Thus, CRISPR/Cas9 inhibits HBV replication and expression in vitro and in vivo and may constitute a new therapeutic strategy for HBV infection.

Indexed as

CRISPR-Cas SystemsAnimalsFemaleGenetic TherapyHepatitis BHepatitis B Surface AntigensHepatitis B virusHep G2 CellsHumansMiceMice, Inbred BALB CMutationHepatitis B Surface Antigens

Identifiers

PMID25652100
OpenAlexW2067119305

What OpenQuestion holds

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Registered trials

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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.