Evidence map›Paper›PMID 19494014›Full record

ArticleJournal of virology2009

Analysis of the percentage of human immunodeficiency virus type 1 sequences that are hypermutated and markers of disease progression in a longitudinal cohort, including one individual with a partially defective Vif.

Anne Piantadosi, Daryl Humes, Bhavna Chohan, R Scott McClelland, Julie Overbaugh

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 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

44 citing papers in PubMed, 73 citations in OpenAlex.

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  10. Absence ofViruses · 2018
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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

5 authors at 3 institutions in 3 countries.

Anne PiantadosiFred Hutchinson Cancer Center, Seattle, WA 98109-1024, USA.
Daryl Humes
Bhavna Chohan
R Scott McClelland
Julie Overbaugh
Fred Hutch Cancer Center · USCritical Path Institute · USUniversity of Nairobi · KE

Funding

University of Washington/Fred Hutch Center for AIDS ResearchP30AI027757 · NIAID · UNIVERSITY OF WASHINGTON · PI Grace C. John-Stewart · 1988 to 2026
$104.9M
University of Washington Medical Scientist Training Program: MD/PhDT32GM007266 · NIGMS · UNIVERSITY OF WASHINGTON · PI HORWITZ, MARSHALL S. · 1985 to 2023
$30.4M
VENEREAL DISEASET32AI007140 · NIAID · UNIVERSITY OF WASHINGTON · PI Julia Cook Dombrowski · 1985 to 2026
$19.4M
EARLY INFECTION IN WOMEN EXPOSED MUCOSALLY TO HIV-1R37AI038518 · NIAID · FRED HUTCHINSON CANCER RESEARCH CENTER · PI OVERBAUGH, JULIE M. · 1999 to 2019
$12.9M
EARLY INFECTION IN WOMEN EXPOSED MUCOSALLY TO HIV-1R01AI038518 · NIAID · UNIVERSITY OF WASHINGTON · PI OVERBAUGH, JULIE M · 1995 to 1998
–
NIAID NIH HHS P30 AI027757NIAID NIH HHS R01 AI38518NIAID NIH HHS R37 AI038518NIAID NIH HHS T32 AI007140NIGMS NIH HHS T32 GM007266NIGMS NIH HHS T32 GM07266
6 · The paper itself

Abstract

Hypermutation, the introduction of excessive G-to-A substitutions by host proteins in the APOBEC family, can impair replication of the human immunodeficiency virus (HIV). Because hypermutation represents a potential antiviral strategy, it is important to determine whether greater hypermutation is associated with slower disease progression in natural infection. We examined the level of HIV-1 hypermutation among 28 antiretroviral-naive Kenyan women at two times during infection. By examining single-copy gag sequences from proviral DNA, hypermutation was detected in 16 of 28 individuals. Among individuals with any hypermutation, a median of 15% of gag sequences were hypermutated (range, 5 to 43%). However, there was no association between the level of gag hypermutation and the viral load or CD4 count. Thus, we observed no overall relationship between hypermutation and markers of disease progression among individuals with low to moderate levels of hypermutation. In addition, one individual sustained a typical viral load despite having a high level of hypermutation. This individual had 43% of gag sequences hypermutated and harbored a partially defective Vif, which was found to permit hypermutation in a peripheral blood mononuclear cell culture. Overall, our results suggest that a potential antiviral therapy based on hypermutation may need to achieve a substantially higher level of hypermutation than is naturally seen in most individuals to impair virus replication and subsequent disease progression.

Indexed as

Disease ProgressionMutationAmino Acid SequenceBase SequenceCells, Culturedenv Gene Products, Human Immunodeficiency VirusFemalegag Gene Products, Human Immunodeficiency VirusHIV-1HIV InfectionsHumansLeukocytes, MononuclearLongitudinal StudiesMolecular Sequence DataMutation, MissenseSequence Alignmentenv Gene Products, Human Immunodeficiency Virusgag Gene Products, Human Immunodeficiency Virusvif Gene Products, Human Immunodeficiency Virusvif protein, Human immunodeficiency virus 1

Identifiers

PMID19494014
PMCPMC2715790
OpenAlexW1978896670

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.