Evidence map›Paper›PMID 33784259›Full record

ArticleJCI insight2021

HIV-1 integration sites in CD4+ T cells during primary, chronic, and late presentation of HIV-1 infection.

Yik Lim Kok, Valentina Vongrad, Sandra E Chaudron, Mohaned Shilaih, Christine Leemann, Kathrin Neumann, Katharina Kusejko, Francesca Di Giallonardo, Herbert Kuster, Dominique L Braun and 3 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
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  16. Molecular Biology and Diversification of Human Retroviruses.Frontiers in virology (Lausanne, Switzerland) · 2022
    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

13 authors at 1 institution in 1 country.

Yik Lim KokDivision of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, and.
Valentina VongradDivision of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, and.
Sandra E ChaudronDivision of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, and.
Mohaned ShilaihDivision of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, and.
Christine LeemannDivision of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, and.
Kathrin NeumannDivision of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, and.
Katharina KusejkoDivision of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, and.
Francesca Di GiallonardoDivision of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, and.
Herbert KusterDivision of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, and.
Dominique L BraunDivision of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, and.
Roger D KouyosDivision of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, and.
Huldrych F GünthardDivision of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, and.
Karin J MetznerDivision of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, and.
University of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HIV-1 is capable of integrating its genome into that of its host cell. We examined the influence of the activation state of CD4+ T cells, the effect of antiretroviral therapy (ART), and the clinical stage of HIV-1 infection on HIV-1 integration site features and selection. HIV-1 integration sites were sequenced from longitudinally sampled resting and activated CD4+ T cells from 12 HIV-1-infected individuals. In total, 589 unique HIV-1 integration sites were analyzed: 147, 391, and 51 during primary, chronic, and late presentation of HIV-1 infection, respectively. As early as during primary HIV-1 infection and independent of the activation state of CD4+ T cells collected on and off ART, HIV-1 integration sites were preferentially detected in recurrent integration genes, genes associated with clonal expansion of latently HIV-1-infected CD4+ T cells, cancer-related genes, and highly expressed genes. The preference for cancer-related genes was more pronounced at late stages of HIV-1 infection. Host genomic features of HIV-1 integration site selection remained stable during HIV-1 infection in both resting and activated CD4+ T cells. In summary, characteristic HIV-1 integration site features are preestablished as early as during primary HIV-1 infection and are found in both resting and activated CD4+ T cells.

Indexed as

Antiretroviral Therapy, Highly ActiveCD4-Positive T-LymphocytesCell ProliferationDisease ProgressionHIV-1HIV InfectionsHost Microbial InteractionsHumansLymphocyte ActivationNeoplasmsViral LoadVirus IntegrationVirus LatencyAIDS/HIVMolecular biologyT cellsVirology

Identifiers

PMID33784259
PMCPMC8262285
OpenAlexW3151387358

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.