Evidence map›Paper›PMID 38638575›Full record

ArticleiScience2024

Longitudinal analysis of genomic mutations in SARS-CoV-2 isolates from persistent COVID-19 patient.

Hiroki Futatsusako, Rina Hashimoto, Masaki Yamamoto, Jumpei Ito, Yasufumi Matsumura, Hajime Yoshifuji, Kotaro Shirakawa, Akifumi Takaori-Kondo, Genotype to Phenotype Japan (G2P-Japan) Consortium, Kei Sato and 2 more

Open access · goldAbstract read
In one paragraph

Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. 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

12 authors at 2 institutions in 1 country.

Hiroki FutatsusakoCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto 6068507, Japan.
Rina HashimotoCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto 6068507, Japan.
Masaki YamamotoDepartment of Clinical Laboratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto 6068507, Japan.
Jumpei ItoDivision of Systems Virology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo 1088639, Japan.
Yasufumi MatsumuraDepartment of Clinical Laboratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto 6068507, Japan.
Hajime YoshifujiDepartment of Rheumatology and Clinical Immunology, Graduate School of Medicine, Kyoto University, Kyoto 6068507, Japan.
Kotaro ShirakawaDepartment of Hematology, Graduate School of Medicine, Kyoto University, Kyoto 6068507, Japan.
Akifumi Takaori-KondoDepartment of Hematology, Graduate School of Medicine, Kyoto University, Kyoto 6068507, Japan.
Genotype to Phenotype Japan (G2P-Japan) Consortium
Kei SatoDivision of Systems Virology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo 1088639, Japan.
Miki NagaoDepartment of Clinical Laboratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto 6068507, Japan.
Kazuo TakayamaCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto 6068507, Japan.
Kyoto University · JPNational Institute of Infectious Diseases · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A primary reason for the ongoing spread of coronavirus disease 2019 (COVID-19) is the continuous acquisition of mutations by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). However, the mechanism of acquiring mutations is not fully understood. In this study, we isolated SARS-CoV-2 from an immunocompromized patient persistently infected with Omicron strain BF.5 for approximately 4 months to analyze its genome and evaluate drug resistance. Although the patient was administered the antiviral drug remdesivir (RDV), there were no acquired mutations in RDV binding site, and all isolates exhibited susceptibility to RDV. Notably, upon analyzing the S protein sequence of the day 119 isolate, we identified mutations acquired by mutant strains emerging from the BF.5 variant, suggesting that viral genome analysis in persistent COVID-19 patients may be useful in predicting viral evolution. These results suggest mutations in SARS-CoV-2 are acquired during long-term viral replication rather than in response to antiviral drugs.

Indexed as

GenomicsMicrobiology and Virology

Identifiers

PMID38638575
PMCPMC11024907
OpenAlexW4393313516

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.