Evidence map›Paper›PMID 22190722›Full record

ArticleJournal of virology2012

Generation of transmitted/founder HIV-1 infectious molecular clones and characterization of their replication capacity in CD4 T lymphocytes and monocyte-derived macrophages.

Christina Ochsenbauer, Tara G Edmonds, Haitao Ding, Brandon F Keele, Julie Decker, Maria G Salazar, Jesus F Salazar-Gonzalez, Robin Shattock, Barton F Haynes, George M Shaw and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 274 papers.

0numbers the graph read from it
0cells of the map it votes in
274citing papers in PubMed
9.4field-weighted citation impact, top 1% 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

274 citing papers in PubMed, 352 citations in OpenAlex.

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214 more citing papers are in PubMed but not listed here.

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 5 institutions in 2 countries.

Christina OchsenbauerDepartment of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Tara G Edmonds
Haitao Ding
Brandon F Keele
Julie Decker
Maria G Salazar
Jesus F Salazar-Gonzalez
Robin Shattock
Barton F Haynes
George M Shaw
Beatrice H Hahn
John C Kappes
University of Alabama at Birmingham · USUniversity of Pennsylvania · USDuke University · USImperial College London · GBScience Applications International Corporation (United States) · US

Funding

Virology CoreP30AI027767 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Renee A. Heffron · 1988 to 2026
$84.1M
Viral and Host Determinants of HIV-1 TransmissionU01AI067854 · NIAID · DUKE UNIVERSITY · PI HAYNES, BARTON F · 2005 to 2005
$14.9M
Mucosal HIV and Immunobiology CenterR24DK064400 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SMITH, PHILLIP D · 2003 to 2012
$4.8M
NIH INTRAMURAL NRSA INSTITUTIONAL TRAINING PROGRAMF35AI007439 · NIAID · U.S. NATIONAL INSTITUTES OF HEALTH · PI KANOF, MARJORIE E · 1985 to 1987
–
NIAID NIH HHS AI007439NIAID NIH HHS P30 AI027767NIAID NIH HHS P30-AI-27767NIAID NIH HHS U01 AI067854NIAID NIH HHS UO1-AI067854NIDDK NIH HHS R24 DK064400NIDDK NIH HHS R24 DK-64400
6 · The paper itself

Abstract

Genome sequences of transmitted/founder (T/F) HIV-1 have been inferred by analyzing single genome amplicons of acute infection plasma viral RNA in the context of a mathematical model of random virus evolution; however, few of these T/F sequences have been molecularly cloned and biologically characterized. Here, we describe the derivation and biological analysis of ten infectious molecular clones, each representing a T/F genome responsible for productive HIV-1 clade B clinical infection. Each of the T/F viruses primarily utilized the CCR5 coreceptor for entry and replicated efficiently in primary human CD4(+) T lymphocytes. This result supports the conclusion that single genome amplification-derived sequences from acute infection allow for the inference of T/F viral genomes that are consistently replication competent. Studies with monocyte-derived macrophages (MDM) demonstrated various levels of replication among the T/F viruses. Although all T/F viruses replicated in MDM, the overall replication efficiency was significantly lower compared to prototypic "highly macrophage-tropic" virus strains. This phenotype was transferable by expressing the env genes in an isogenic proviral DNA backbone, indicating that T/F virus macrophage tropism mapped to Env. Furthermore, significantly higher concentrations of soluble CD4 were required to inhibit T/F virus infection compared to prototypic macrophage-tropic virus strains. Our findings suggest that the acquisition of clinical HIV-1 subtype B infection occurs by mucosal exposure to virus that is not highly macrophage tropic and that the generation and initial biological characterization of 10 clade B T/F infectious molecular clones provides new opportunities to probe virus-host interactions involved in HIV-1 transmission.

Indexed as

Virus ReplicationCD4-Positive T-LymphocytesCells, CulturedFemaleGenome, ViralHIV-1HIV InfectionsHumansMacrophagesMaleMolecular Sequence Data

Identifiers

PMID22190722
PMCPMC3302286
OpenAlexW1983262897

What OpenQuestion holds

Textmetadata
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.