Evidence map›Paper›PMID 31218578›Full record

ArticleClinical and experimental medicine2019

Direct antiviral agents upregulate natural killer cell potential activity in chronic hepatitis C patients.

Han-Ji Jiang, Xiao-Xiao Wang, Bi-Fen Luo, Xu Cong, Qian Jin, Hong Qin, Hai-Ying Zhang, Xiang-Sha Kong, Lai Wei, Bo Feng

Abstract read
PubMed Publisher
In one paragraph

Article in Clinical and experimental medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
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  5. Lymphocyte Landscape after ChronicInternational journal of molecular sciences · 2020
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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 1 institution in 1 country.

Han-Ji JiangBeijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Diseases, Peking University Hepatology Institute, Peking University People's Hospital, No. 11 Xizhimen South Street, Beijing, 100044, People's Republic of China.
Xiao-Xiao WangBeijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Diseases, Peking University Hepatology Institute, Peking University People's Hospital, No. 11 Xizhimen South Street, Beijing, 100044, People's Republic of China.
Bi-Fen LuoBeijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Diseases, Peking University Hepatology Institute, Peking University People's Hospital, No. 11 Xizhimen South Street, Beijing, 100044, People's Republic of China.
Xu CongBeijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Diseases, Peking University Hepatology Institute, Peking University People's Hospital, No. 11 Xizhimen South Street, Beijing, 100044, People's Republic of China.
Qian JinBeijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Diseases, Peking University Hepatology Institute, Peking University People's Hospital, No. 11 Xizhimen South Street, Beijing, 100044, People's Republic of China.
Hong QinBeijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Diseases, Peking University Hepatology Institute, Peking University People's Hospital, No. 11 Xizhimen South Street, Beijing, 100044, People's Republic of China.
Hai-Ying ZhangBeijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Diseases, Peking University Hepatology Institute, Peking University People's Hospital, No. 11 Xizhimen South Street, Beijing, 100044, People's Republic of China.
Xiang-Sha KongBeijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Diseases, Peking University Hepatology Institute, Peking University People's Hospital, No. 11 Xizhimen South Street, Beijing, 100044, People's Republic of China.
Lai WeiBeijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Diseases, Peking University Hepatology Institute, Peking University People's Hospital, No. 11 Xizhimen South Street, Beijing, 100044, People's Republic of China.
Bo FengBeijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Diseases, Peking University Hepatology Institute, Peking University People's Hospital, No. 11 Xizhimen South Street, Beijing, 100044, People's Republic of China. fengbo@pkuph.edu.cn.ORCID http://orcid.org/0000-0001-5084-6715
Peking University · CN

Funding

National S&T Major Projects for Infectious Diseases Control (CN) 2017ZX10203202-003-003National S&T Major Projects for Infectious Diseases Control (CN) 2017ZX10302201-004-001
6 · The paper itself

Abstract

Direct antiviral agents (DAAs) can eliminate hepatitis C virus rapidly and make chronic hepatitis C (CHC) curable. The changes in the innate immune system during treatment with DAAs are still in dispute. To investigate how the functions of natural killer (NK) cells change during and after treatment with DAAs in each NK cell subset. Thirteen CHC patients were treated with sofosbuvir/ledipasvir, and the expression levels of NKp46 and NKG2A were tested via flow cytometry at baseline, at 2, 4, 8 and 12 weeks during the therapy and 12 and 24 weeks after the end of treatment; expression levels were compared between CHC patients and 13 healthy controls. A redirected killing assay was used to detect the cytotoxicity of NK cells. After coculturing NK cells with JFH-Huh7 cells for 72 h, HCV RNA was tested to analyze the inhibition ability of NK cells. All patients achieved sustained virologic response. The expression of the activating receptor NKp46 was decreased first at week 8 during therapy with DAAs and then increased and normalized to levels in healthy controls after treatment with DAAs. The expression of the inhibitory receptor NKG2A was decreased during and after treatment with DAAs. Each NK cell subset has a similar changing trend during and after treatment with DAAs, although some differences can be found earlier and later. The ratio of NKp46 and NKG2A was upregulated after treatment with DAAs. CD56

Indexed as

Immunity, InnateAdultAntiviral AgentsBenzimidazolesFemaleFluorenesHepatitis C, ChronicHumansKiller Cells, NaturalLongitudinal StudiesMaleMiddle AgedNatural Cytotoxicity Triggering Receptor 1NK Cell Lectin-Like Receptor Subfamily CSofosbuvirTime FactorsAntiviral AgentsBenzimidazolesFluorenesKLRC1 protein, humanledipasvirNatural Cytotoxicity Triggering Receptor 1NCR1 protein, humanNK Cell Lectin-Like Receptor Subfamily CSofosbuvirDirect antiviral agentsFunctionHepatitis C virusInnate immune systemNatural killer cells

Identifiers

PMID31218578
OpenAlexW2949221538

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.