Evidence map›Paper›PMID 19300501›Full record

ArticlePLoS genetics2009

Genetic drift of HIV populations in culture.

Yegor Voronin, Sarah Holte, Julie Overbaugh, Michael Emerman

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.7field-weighted citation impact, top 34% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Immune Ecosystem of Virus-Infected Host Tissues.International journal of molecular sciences · 2018
    Review
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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

4 authors at 2 institutions in 2 countries.

Yegor VoroninHuman Biology Division, Fred Hutchinson Cancer Research Center, Seattle, WA, USA. yvoronin@fhcrc.org
Sarah Holte
Julie Overbaugh
Michael Emerman
Fred Hutch Cancer Center · USCape Town HVTN Immunology Laboratory / Hutchinson Centre Research Institute of South Africa · ZA

Funding

University of Washington/Fred Hutch Center for AIDS ResearchP30AI027757 · NIAID · UNIVERSITY OF WASHINGTON · PI Grace C. John-Stewart · 1988 to 2026
$104.9M
VPR AND HIV INFECTIONR37AI030927 · NIAID · FRED HUTCHINSON CANCER RESEARCH CENTER · PI EMERMAN, MICHAEL · 2001 to 2010
$4.6M
LENTIVIRAL VARIATION AND AIDSR01AI034251 · NIAID · UNIVERSITY OF WASHINGTON · PI OVERBAUGH, JULIE M. · 1993 to 2008
$2.8M
Mathematical and Experimental Models for HIV DynamicsR01AI055343 · NIAID · FRED HUTCHINSON CANCER RESEARCH CENTER · PI HOLTE, SARAH E · 2003 to 2007
$1.7M
HIV Infection of Non-Dividing CellsR01AI073085 · NIAID · FRED HUTCHINSON CANCER RESEARCH CENTER · PI EMERMAN, MICHAEL · 2007 to 2010
$1.4M
NIAID NIH HHS P30 AI027757NIAID NIH HHS P30 AI 27757NIAID NIH HHS R01 AI034251NIAID NIH HHS R01 AI055343NIAID NIH HHS R01 AI073085NIAID NIH HHS R01 AI34251NIAID NIH HHS R37 AI030927
6 · The paper itself

Abstract

Populations of Human Immunodeficiency Virus type 1 (HIV-1) undergo a surprisingly large amount of genetic drift in infected patients despite very large population sizes, which are predicted to be mostly deterministic. Several models have been proposed to explain this phenomenon, but all of them implicitly assume that the process of virus replication itself does not contribute to genetic drift. We developed an assay to measure the amount of genetic drift for HIV populations replicating in cell culture. The assay relies on creation of HIV populations of known size and measurements of variation in frequency of a neutral allele. Using this assay, we show that HIV undergoes approximately ten times more genetic drift than would be expected from its population size, which we defined as the number of infected cells in the culture. We showed that a large portion of the increase in genetic drift is due to non-synchronous infection of target cells. When infections are synchronized, genetic drift for the virus is only 3-fold higher than expected from its population size. Thus, the stochastic nature of biological processes involved in viral replication contributes to increased genetic drift in HIV populations. We propose that appreciation of these effects will allow better understanding of the evolutionary forces acting on HIV in infected patients.

Indexed as

Genetic DriftCells, CulturedGene FrequencyHIV-1HIV InfectionsHumansModels, GeneticStochastic ProcessesVirus Replication

Identifiers

PMID19300501
PMCPMC2652835
OpenAlexW1984727612

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.