Evidence map›Paper›PMID 30584239›Full record

ArticleScientific reports2018

Expansion of viral variants associated with immune escape and impaired virion secretion in patients with HBV reactivation after resolved infection.

Tadashi Inuzuka, Yoshihide Ueda, Soichi Arasawa, Haruhiko Takeda, Tomonori Matsumoto, Yukio Osaki, Shinji Uemoto, Hiroshi Seno, Hiroyuki Marusawa

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. 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
1.9field-weighted citation impact, top 13% 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, 17 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
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 3 institutions in 1 country.

Tadashi InuzukaDepartment of Gastroenterology and Hepatology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Yoshihide UedaDepartment of Gastroenterology and Hepatology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Soichi ArasawaDepartment of Gastroenterology and Hepatology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Haruhiko TakedaDepartment of Gastroenterology and Hepatology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Tomonori MatsumotoDepartment of Gastroenterology and Hepatology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID http://orcid.org/0000-0003-4483-2178
Yukio OsakiDepartment of Gastroenterology and Hepatology, Osaka Red Cross Hospital, Osaka, Japan.
Shinji UemotoDepartment of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Hiroshi SenoDepartment of Gastroenterology and Hepatology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Hiroyuki MarusawaDepartment of Gastroenterology and Hepatology, Graduate School of Medicine, Kyoto University, Kyoto, Japan. maru@kuhp.kyoto-u.ac.jp.
Kyoto University · JPJapan Society for the Promotion of Science · JPOsaka Red Cross Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HBV reactivation could be induced under immunosuppressive conditions in patients with resolved infection. This study aimed to clarify the viral factors associated with the pathogenesis of HBV reactivation in association with the immunosuppressive status. Whole HBV genome sequences were determined from the sera of 24 patients with HBV reactivation, including 8 cases under strong immunosuppression mediated by hematopoietic stem cell transplantation (HSCT) and 16 cases without HSCT. Ultra-deep sequencing revealed that the prevalence of genotype B and the ratio of non-synonymous to synonymous evolutionary changes in the surface (S) gene were significantly higher in non-HSCT cases than in patients with HSCT. Those non-synonymous variants included immune escape (6/16 cases) and MHC class II-restricted T-cell epitope variants (6/16 cases). Furthermore, reactivated HBV in 11 of 16 (69%) non-HSCT cases possessed substitutions associated with impaired virion secretion, including E2G, L77R, L98V, T118K, and Q129H in the S region, and M1I/V in the PreS2 region. In conclusion, virologic features of reactivated HBV clones differed depending on the intensity of the immunosuppressive condition. HBV reactivation triggered by immunosuppressive conditions, especially those without HSCT, was characterized by the expansion of variants associated with immune escape, MHC class II-restricted T-cell epitope alterations, and/or impaired virion secretion.

Indexed as

Immune EvasionPolymorphism, GeneticAgedAged, 80 and overFemaleHepatitis BHepatitis B virusHumansMaleMiddle Aged

Identifiers

PMID30584239
PMCPMC6305382
OpenAlexW2905890016

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.