Evidence map›Paper›PMID 20174636›Full record

ArticlePloS one2010

Restricted genetic diversity of HIV-1 subtype C envelope glycoprotein from perinatally infected Zambian infants.

Hong Zhang, Damien C Tully, Federico G Hoffmann, Jun He, Chipepo Kankasa, Charles Wood

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

25 citing papers in PubMed, 43 citations in OpenAlex.

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  18. Analysis of primary resistance mutations to HIV-1 entry inhibitors in therapy naive subtype C HIV-1 infected mother-infant pairs from Zambia.Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology · 2013
    Article
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4 · The record

Corrections and comments

  • Erratum issued
  • Erratum issued
5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Hong ZhangNebraska Center for Virology, University of Nebraska, Lincoln, Nebraska, United States of America.
Damien C Tully
Federico G Hoffmann
Jun He
Chipepo Kankasa
Charles Wood
University of Nebraska–Lincoln · USUniversity Teaching Hospital · ZM

Funding

VIRAL SHUTOFF OF HOST TRANSCRIPTION--PBCV-1 INFECTEDP20RR015635 · NCRR · UNIVERSITY OF NEBRASKA LINCOLN · PI KUSZYNSKI, CHARLES ARTHUR · 2000 to 2009
$22.1M
KAPOSIS SARCOMA AND HUMAN HERPESVIRUS IN AFRICAR01CA075903 · NCI · UNIVERSITY OF NEBRASKA LINCOLN · PI WOOD, CHARLES · 1998 to 2015
$11.1M
Supplement: Fogarty Training in HIV- and AIDS Associated Diseases/MalignanciesD43TW001429 · FIC · UNIVERSITY OF NEBRASKA LINCOLN · PI WOOD, CHARLES · 2000 to 2015
$7.2M
FIC NIH HHS D43 TW001429FIC NIH HHS TW001429NCI NIH HHS CA75903NCI NIH HHS R01 CA075903NCRR NIH HHS P20 RR015635NCRR NIH HHS P20 RR15635NCRR NIH HHS RR15635
6 · The paper itself

Abstract

backgroundMother-to-child transmission of HIV-1 remains a significant problem in the resource-constrained settings where anti-retroviral therapy is still not widely available. Understanding the earliest events during HIV-1 transmission and characterizing the newly transmitted or founder virus is central to intervention efforts. In this study, we analyzed the viral env quasispecies of six mother-infant transmission pairs (MIPs) and characterized the genetic features of envelope glycoprotein that could influence HIV-1 subtype C perinatal transmission. METHODOLOGY AND

findingsThe V1-V5 region of env was amplified from 6 MIPs baseline samples and 334 DNA sequences in total were analyzed. A comparison of the viral population derived from the mother and infant revealed a severe genetic bottleneck occurring during perinatal transmission, which was characterized by low sequence diversity in the infant. Phylogenetic analysis indicates that most likely in all our infant subjects a single founder virus was responsible for establishing infection. Furthermore, the newly transmitted viruses from the infant had significantly fewer potential N-linked glycosylation sites in Env V1-V5 region and showed a propensity to encode shorter variable loops compared to the nontransmitted viruses. In addition, a similar intensity of selection was seen between mothers and infants with a higher rate of synonymous (dS) compared to nonsynonymous (dN) substitutions evident (dN/dS<1).

conclusionsOur results indicate that a strong genetic bottleneck occurs during perinatal transmission of HIV-1 subtype C. This is evident through population diversity and phylogenetic patterns where a single viral variant appears to be responsible for infection in the infants. As a result the newly transmitted viruses are less diverse and harbored significantly less glycosylated envelope. This suggests that viruses with the restricted glycosylation in envelope glycoprotein appeared to be preferentially transmitted during HIV-1 subtype C perinatal transmission. In addition, our findings also indicated that purifying selection appears to predominate in shaping the early intrahost evolution of HIV-1 subtype C envelope sequences.

Indexed as

Genetic VariationInfectious Disease Transmission, VerticalFemaleGene Products, envHIV-1HIV InfectionsHumansInfantInfant, NewbornPhylogenyPregnancyPregnancy Complications, InfectiousSequence Analysis, DNAZambiaGene Products, env

Identifiers

PMID20174636
PMCPMC2823783
OpenAlexW2170830827

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.