Evidence map›Paper›PMID 19625411›Full record

ArticleJournal of virology2009

Human immunodeficiency virus type 1 V1-to-V5 envelope variants from the chronic phase of infection use CCR5 and fuse more efficiently than those from early after infection.

Behzad Etemad, Angela Fellows, Brenda Kwambana, Anupa Kamat, Yang Feng, Sandra Lee, Manish Sagar

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

33 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. iScience · 2023
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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

7 authors at 3 institutions in 1 country.

Behzad EtemadDepartment of Medicine, Brigham and Women's Hospital, Harvard Medical School, Cambridge, Massachusetts 02139, USA.
Angela Fellows
Brenda Kwambana
Anupa Kamat
Yang Feng
Sandra Lee
Manish Sagar
Harvard University · USBrigham and Women's Hospital · USDana-Farber Cancer Institute · US

Funding

Genotypic and Phenotypic Characterization of Heterosexually Transmitted HIV-1R01AI077473 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI SAGAR, MANISH · 2008 to 2011
$1.4M
NIAID NIH HHS AI1077473NIAID NIH HHS R01 AI077473
6 · The paper itself

Abstract

Human immunodeficiency virus type 1 (HIV-1) envelope glycoprotein modifications over the course of infection have been associated with coreceptor switching and antibody neutralization resistance, but the effect of the changes on replication and host cell receptor usage remains unclear. To examine this question, unique early- and chronic-stage infection envelope V1-to V5 (V1-V5) segments from eight HIV-1 subtype A-infected subjects were incorporated into an isogenic background to construct replication-competent recombinant viruses. In all subjects, viruses with chronic-infection V1-V5 segments showed greater replication capacity than those with early-infection V1-V5 domains in cell lines with high levels of both the CD4 and the CCR5 receptors. Viruses with chronic-infection V1-V5s demonstrated a significantly increased ability to replicate in cells with low CCR5 receptor levels and greater resistance to CCR5 receptor and fusion inhibitors compared to those with early-infection V1-V5 segments. These properties were associated with sequence changes in the envelope V1-V3 segments. Viruses with the envelope segments from the two infection time points showed no significant difference in their ability to infect cells with low CD4 receptor densities, in their sensitivity to soluble CD4, or in their replication capacity in monocyte-derived macrophages. Our results suggest that envelope changes, primarily in the V1-V3 domains, increase both the ability to use the CCR5 receptor and fusion kinetics. Thus, envelope modifications over time within a host potentially enhance replication capacity.

Indexed as

CD4 AntigensCell LineGenotypeHIV-1HIV InfectionsHumansInhibitory Concentration 50KineticsMacrophagesModels, BiologicalMonocytesPolymerase Chain ReactionProtein Structure, TertiaryReceptors, CCR5Viral Envelope ProteinsCD4 AntigensReceptors, CCR5Viral Envelope Proteins

Identifiers

PMID19625411
PMCPMC2748008
OpenAlexW2155445576

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.