Evidence map›Paper›PMID 32685701›Full record

ArticleHealth science reports2020

Decreased expression of interferon-stimulated genes in B cells of patients with chronic hepatitis C during interferon-free therapy potentially suggests the eradication of hepatitis C virus in the B cells: A cohort study.

Jun Arai, Takayoshi Ito, Yuu Shimozuma, Manabu Uchikoshi, Yoko Nakajima, Masashi Sakaki, Shojiro Uozumi, Atsushi Kajiwara, Ikuya Sugiura, Yumi Otoyama and 8 more

Open access · goldAbstract read
In one paragraph

Article in Health science reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 39% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
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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

18 authors at 2 institutions in 1 country.

Jun AraiDepartment of Medicine, Division of Gastroenterology Showa University School of Medicine Tokyo Japan.
Takayoshi ItoDigestive Disease Center Showa University Koto Toyosu Hospital Tokyo Japan.ORCID https://orcid.org/0000-0001-9854-4257
Yuu ShimozumaDepartment of Medicine, Division of Gastroenterology Showa University School of Medicine Tokyo Japan.
Manabu UchikoshiDepartment of Medicine, Division of Gastroenterology Showa University School of Medicine Tokyo Japan.
Yoko NakajimaDepartment of Medicine, Division of Gastroenterology Showa University School of Medicine Tokyo Japan.
Masashi SakakiDepartment of Medicine, Division of Gastroenterology Showa University School of Medicine Tokyo Japan.
Shojiro UozumiDepartment of Medicine, Division of Gastroenterology Showa University School of Medicine Tokyo Japan.
Atsushi KajiwaraDepartment of Medicine, Division of Gastroenterology Showa University School of Medicine Tokyo Japan.
Ikuya SugiuraDepartment of Medicine, Division of Gastroenterology Showa University School of Medicine Tokyo Japan.
Yumi OtoyamaDepartment of Medicine, Division of Gastroenterology Showa University School of Medicine Tokyo Japan.
Hisako NozawaDepartment of Medicine, Division of Gastroenterology Showa University School of Medicine Tokyo Japan.
Toshikazu KuriharaInternal Medicine Showa University Karasuyama Hospital Tokyo Japan.
Junichi EguchiDigestive Disease Center Showa University Koto Toyosu Hospital Tokyo Japan.
Norihiro NomuraDigestive Disease Center Showa University Koto Toyosu Hospital Tokyo Japan.
Dai SakumaDigestive Disease Center Showa University Koto Toyosu Hospital Tokyo Japan.
Masashi SatoDigestive Disease Center Showa University Koto Toyosu Hospital Tokyo Japan.
Yoshio DeguchiDigestive Disease Center Showa University Koto Toyosu Hospital Tokyo Japan.
Hitoshi YoshidaDepartment of Medicine, Division of Gastroenterology Showa University School of Medicine Tokyo Japan.
Showa University · JPShowa University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsHepatitis C virus (HCV) infection is monitored by the host innate immunity that includes the endogenous interferon (IFN), which up-regulates IFN-stimulated genes (ISGs). HCV is both hepatotropic and lymphotropic, but HCV replication in lymphoid cells is a controversial issue. Here, we analyzed the mRNA levels of the ISGs in B cells of HCV-infected patients during antiviral therapy and investigated the effects of viral eradication.

methodsOne hundred and eighty-one patients with chronic hepatitis C and 26 healthy volunteers were enrolled in this study. Levels of HCV RNA and mRNA of ISGs in B cells isolated from the patients were monitored before, during, and after antiviral therapy.

resultsHCV RNA was detected in B cells of 133/175 (76.0%) patients who achieved sustained virologic response (SVR) before therapy was started. The positive ratio of HCV RNA in B cells was higher in patients with genotype 1 and the non-major genotype of interleukin 28B. HCV RNA in B cells of most patients disappeared 1 week after antiviral therapy was started. The baseline expression of ISG mRNA was significantly higher in the patients than in the healthy volunteers. Levels of ISG mRNA were increased and remained high throughout the IFN-based therapy. In contrast, levels of ISG mRNA in patients who achieved SVR were significantly decreased 1 week after the IFN-free therapy was started and remained low during the therapy.

conclusionsThese results suggested that IFN-free therapy potentially eradicated HCV in the B cells, leading to the down-regulation of endogenous ISGs. The level of ISG mRNA could be used as a marker for viral eradication in B cells.

Indexed as

anti‐hepatitis C virus DAA (directly acting antivirals)B cellhepatitis C virusinterferonstissue tropism

Identifiers

PMID32685701
PMCPMC7362757
OpenAlexW3043284228

What OpenQuestion holds

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LicenceCC BY-NC
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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.