Evidence map›Paper›PMID 23691172›Full record

ArticlePloS one2013

A single HIV-1 cluster and a skewed immune homeostasis drive the early spread of HIV among resting CD4+ cell subsets within one month post-infection.

Charline Bacchus, Antoine Cheret, Véronique Avettand-Fenoël, Georges Nembot, Adeline Mélard, Catherine Blanc, Caroline Lascoux-Combe, Laurence Slama, Thierry Allegre, Clotilde Allavena and 11 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

37 citing papers in PubMed, 69 citations in OpenAlex.

  1. Trial
  2. HIV-1 DNA decay dynamics in blood during more than a decade of suppressive antiretroviral therapy.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2014
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  15. Naive CD4+ T Cells Harbor a Large Inducible Reservoir of Latent, Replication-competent Human Immunodeficiency Virus Type 1.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2019
    Article
  16. Article
  17. Article
  18. A CCR5BMC research notes · 2019
    Article
  19. Article
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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

21 authors at 11 institutions in 1 country.

Charline BacchusPierre-and-Marie-Curie University Paris 06, Laboratory Immunity and Infection UMR_S 945, F-75013, Paris, France.
Antoine Cheret
Véronique Avettand-Fenoël
Georges Nembot
Adeline Mélard
Catherine Blanc
Caroline Lascoux-Combe
Laurence Slama
Thierry Allegre
Clotilde Allavena
Yazdan Yazdanpanah
Claudine Duvivier
Christine Katlama
Cécile Goujard
Bao Chau Phung Seksik
Anne Leplatois
Jean-Michel Molina
Laurence Meyer
Brigitte Autran
Christine Rouzioux
OPTIPRIM ANRS 147 study group
Inserm · FRAssistance Publique – Hôpitaux de Paris · FRDélégation Paris 5 · FRSorbonne Université · FRUniversité Paris Cité · FRCentre Hospitalier de Tourcoing · FRCentre Hospitalier du Pays d'Aix · FRHôpital l'Archet · FRHôpital Tenon · FRInstitut Pasteur · FRPitié-Salpêtrière Hospital · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Optimizing therapeutic strategies for an HIV cure requires better understanding the characteristics of early HIV-1 spread among resting CD4+ cells within the first month of primary HIV-1 infection (PHI). We studied the immune distribution, diversity, and inducibility of total HIV-DNA among the following cell subsets: monocytes, peripheral blood activated and resting CD4 T cells, long-lived (naive [TN] and central-memory [TCM]) and short-lived (transitional-memory [TTM] and effector-memory cells [TEM]) resting CD4+T cells from 12 acutely-infected individuals recruited at a median 36 days from infection. Cells were sorted for total HIV-DNA quantification, phylogenetic analysis and inducibility, all studied in relation to activation status and cell signaling. One month post-infection, a single CCR5-restricted viral cluster was massively distributed in all resting CD4+ subsets from 88% subjects, while one subject showed a slight diversity. High levels of total HIV-DNA were measured among TN (median 3.4 log copies/million cells), although 10-fold less (p = 0.0005) than in equally infected TCM (4.5), TTM (4.7) and TEM (4.6) cells. CD3-CD4+ monocytes harbored a low viral burden (median 2.3 log copies/million cells), unlike equally infected resting and activated CD4+ T cells (4.5 log copies/million cells). The skewed repartition of resting CD4 subsets influenced their contribution to the pool of resting infected CD4+T cells, two thirds of which consisted of short-lived TTM and TEM subsets, whereas long-lived TN and TCM subsets contributed the balance. Each resting CD4 subset produced HIV in vitro after stimulation with anti-CD3/anti-CD28+IL-2 with kinetics and magnitude varying according to subset differentiation, while IL-7 preferentially induced virus production from long-lived resting TN cells. In conclusion, within a month of infection, a clonal HIV-1 cluster is massively distributed among resting CD4 T-cell subsets with a flexible inducibility, suggesting that subset activation and skewed immune homeostasis determine the conditions of viral dissemination and early establishment of the HIV reservoir.

Indexed as

AdultCD4-Positive T-LymphocytesDNA, ViralFemaleHIV-1HIV InfectionsHomeostasisHumansMaleMiddle AgedTime FactorsT-Lymphocyte SubsetsViral LoadYoung AdultDNA, Viral

Identifiers

PMID23691172
PMCPMC3653877
OpenAlexW2074579395

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.