Evidence map›Paper›PMID 28761140›Full record

ArticleScientific reports2017

Dynamics and mechanisms of clonal expansion of HIV-1-infected cells in a humanized mouse model.

Yorifumi Satou, Hiroo Katsuya, Asami Fukuda, Naoko Misawa, Jumpei Ito, Yoshikazu Uchiyama, Paola Miyazato, Saiful Islam, Ariberto Fassati, Anat Melamed and 3 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.2field-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

18 citing papers in PubMed, 36 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 5 institutions in 2 countries.

Yorifumi SatouInternational Research Center for Medical Sciences (IRCMS), Kumamoto University, Kumamoto, 860-0811, Japan. y-satou@kumamoto-u.ac.jp.ORCID 0000-0002-1495-7810
Hiroo KatsuyaInternational Research Center for Medical Sciences (IRCMS), Kumamoto University, Kumamoto, 860-0811, Japan.
Asami FukudaInternational Research Center for Medical Sciences (IRCMS), Kumamoto University, Kumamoto, 860-0811, Japan.
Naoko MisawaLaboratory of Systems Virology, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto, 606-8507, Japan.
Jumpei ItoDivision of Human Genetics, Department of Integrated Genetics, National Institute of Genetics, Shizuoka, 411-8540, Japan.
Yoshikazu UchiyamaDepartment of Medical Physics, Faculty of Life Sciences, Kumamoto University, Kumamoto, 862-0976, Japan.
Paola MiyazatoInternational Research Center for Medical Sciences (IRCMS), Kumamoto University, Kumamoto, 860-0811, Japan.
Saiful IslamInternational Research Center for Medical Sciences (IRCMS), Kumamoto University, Kumamoto, 860-0811, Japan.
Ariberto FassatiDivision of Infection and Immunity, University College London, London, WC1E 6BT, United Kingdom.
Anat MelamedDepartment of Immunology, Division of Infectious Diseases, Imperial College London, London, W2 1PG, United Kingdom.
Charles R M BanghamDepartment of Immunology, Division of Infectious Diseases, Imperial College London, London, W2 1PG, United Kingdom.
Yoshio KoyanagiLaboratory of Systems Virology, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto, 606-8507, Japan.
Kei SatoLaboratory of Systems Virology, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto, 606-8507, Japan.ORCID 0000-0003-4431-1380
Kumamoto University · JPKyoto University · JPImperial College London · GBNational Institute of Genetics · JPUniversity College London · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

Combination anti-retroviral therapy (cART) has drastically improved the clinical outcome of HIV-1 infection. Nonetheless, despite effective cART, HIV-1 persists indefinitely in infected individuals. Clonal expansion of HIV-1-infected cells in peripheral blood has been reported recently. cART is effective in stopping the retroviral replication cycle, but not in inhibiting clonal expansion of the infected host cells. Thus, the proliferation of HIV-1-infected cells may play a role in viral persistence, but little is known about the kinetics of the generation, the tissue distribution or the underlying mechanism of clonal expansion in vivo. Here we analyzed the clonality of HIV-1-infected cells using high-throughput integration site analysis in a hematopoietic stem cell-transplanted humanized mouse model. Clonally expanded, HIV-1-infected cells were detectable at two weeks post infection, their abundance increased with time, and certain clones were present in multiple organs. Expansion of HIV-1-infected clones was significantly more frequent when the provirus was integrated near host genes in specific gene ontological classes, including cell activation and chromatin regulation. These results identify potential drivers of clonal expansion of HIV-1-infected cells in vivo.

Indexed as

AnimalsCD4-Positive T-LymphocytesCell ProliferationCells, CulturedClone CellsDisease Models, AnimalGene Regulatory NetworksHigh-Throughput Nucleotide SequencingHIV-1HIV InfectionsHumansJurkat CellsLymphocyte ActivationMiceRNA, ViralSequence Analysis, RNARNA, Viral

Identifiers

PMID28761140
PMCPMC5537293
OpenAlexW2736845447

What OpenQuestion holds

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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.