Evidence map›Paper›PMID 21191008›Full record

ArticleJournal of virology2011

Origin and evolution of HIV-1 in breast milk determined by single-genome amplification and sequencing.

Jesus F Salazar-Gonzalez, Maria G Salazar, Gerald H Learn, Genevieve G Fouda, Helen H Kang, Tatenda Mahlokozera, Andrew B Wilks, Rachel V Lovingood, Andrea Stacey, Linda Kalilani and 9 more

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

46 citing papers in PubMed, 64 citations in OpenAlex.

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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

19 authors at 8 institutions in 3 countries.

Jesus F Salazar-GonzalezDivision of Viral Pathogenesis, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, E/CLS1028, Boston, MA 02115, USA.
Maria G Salazar
Gerald H Learn
Genevieve G Fouda
Helen H Kang
Tatenda Mahlokozera
Andrew B Wilks
Rachel V Lovingood
Andrea Stacey
Linda Kalilani
Steve R Meshnick
Persephone Borrow
David C Montefiori
Thomas N Denny
Norman L Letvin
George M Shaw
Beatrice H Hahn
Sallie R Permar
Center for HIV/AIDS Vaccine Immunology A0167854
University of Alabama at Birmingham · USDuke University · USHarvard University · USBeth Israel Deaconess Medical Center · USJenner Institute · GBUniversity of Malawi · MWUniversity of North Carolina at Chapel Hill · USUniversity of Oxford · GB

Funding

Viral and Host Determinants of HIV-1 TransmissionU01AI067854 · NIAID · DUKE UNIVERSITY · PI LETVIN, NORMAN L · 2005 to 2005
$14.9M
SIV-specific Immunity in breast milk during infection and after vaccinationK08AI087992 · NIAID · DUKE UNIVERSITY · PI PERMAR, SALLIE R. · 2009 to 2013
$568k
NIAID NIH HHS K08 AI087992NIAID NIH HHS K08AI087992NIAID NIH HHS R01AI067854NIAID NIH HHS U01 AI067854
6 · The paper itself

Abstract

HIV transmission via breastfeeding accounts for a considerable proportion of infant HIV acquisition. However, the origin and evolution of the virus population in breast milk, the likely reservoir of transmitted virus variants, are not well characterized. In this study, HIV envelope (env) genes were sequenced from virus variants amplified by single-genome amplification from plasmas and milk of 12 chronically HIV-infected, lactating Malawian women. Maximum likelihood trees and statistical tests of compartmentalization revealed interspersion of plasma and milk HIV env sequences in the majority of subjects, indicating limited or no compartmentalization of milk virus variants. However, phylogenetic tree analysis further revealed monotypic virus variants that were significantly more frequent in milk (median proportion of identical viruses, 29.5%; range, 0 to 61%) than in plasma (median proportion of identical viruses, 0%; range, 0 to 26%) (P = 0.002), suggesting local virus replication in the breast milk compartment. Moreover, clonally amplified virus env genes in milk produced functional virus Envs that were all CCR5 tropic. Milk and plasma virus Envs had similar predicted phenotypes and neutralization sensitivities to broadly neutralizing antibodies in both transmitting and nontransmitting mothers. Finally, phylogenetic comparison of longitudinal milk and plasma virus env sequences revealed synchronous virus evolution and new clonal amplification of evolved virus env genes in milk. The limited compartmentalization and the clonal amplification of evolving, functional viruses in milk indicate continual seeding of the mammary gland by blood virus variants, followed by transient local replication of these variants in the breast milk compartment.

Indexed as

Evolution, MolecularGenetic VariationCluster Analysisenv Gene Products, Human Immunodeficiency VirusFemaleHIV-1HIV InfectionsHumansInfantInfant, NewbornMalawiMilk, HumanMolecular Sequence DataPhylogenyPlasmaPregnancyenv Gene Products, Human Immunodeficiency VirusReceptors, CCR5Receptors, HIVRNA, Viral

Identifiers

PMID21191008
PMCPMC3067940
OpenAlexW2097948558

What OpenQuestion holds

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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.