Evidence map›Paper›PMID 15890925›Full record

ArticleJournal of virology2005

Effect of polypurine tract (PPT) mutations on human immunodeficiency virus type 1 replication: a virus with a completely randomized PPT retains low infectivity.

Lesa R Miles, Beth E Agresta, Mahfuz B Khan, Shixing Tang, Judith G Levin, Michael D Powell

Abstract read
In one paragraph

Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Notable reduction in illegitimate integration mediated by a PPT-deleted, nonintegrating lentiviral vector.Molecular therapy : the journal of the American Society of Gene Therapy · 2011
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
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  15. Article
  16. Article
  17. Article
  18. Review
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

6 authors at 2 institutions in 1 country.

Lesa R MilesDepartment of Microbiology, Biochemistry and Immunology, Morehouse School of Medicine, 720 Westview Dr. S. W., Atlanta, GA 30310, USA.
Beth E Agresta
Mahfuz B Khan
Shixing Tang
Judith G Levin
Michael D Powell
Eunice Kennedy Shriver National Institute of Child Health and Human Development · USMorehouse School of Medicine · US

Funding

TRANSCRIPTION FACTORS AND PROSTATE CANCERG12RR003034 · NCRR · MOREHOUSE SCHOOL OF MEDICINE · PI POWELL, MICHAEL D · 1986 to 2011
$32.4M
Vascular Cell Apoptosis: Mediator Role of Transforming Growth Factor-beta-1S06GM008248 · NIGMS · MOREHOUSE SCHOOL OF MEDICINE · PI YANG, QINGLIN · 1989 to 2009
$19.8M
Molecular Genetics Of Mammalian Retrovirus ReplicationZIAHD000069 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI LEVIN, JUDITH G · 2009 to 2015
$7.2M
MOLECULAR GENETICS OF MAMMALIAN RETROVIRUS REPLICATIONZ01HD000069 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI LEVIN, JUDITH G · 1985 to 2008
$1.8M
Sequence requirements for the HIV-1 PPTF31GM065793 · NIGMS · MOREHOUSE SCHOOL OF MEDICINE · PI BLACK, LESA R · 2001 to 2005
$111k
NCRR NIH HHS G12 RR003034NCRR NIH HHS G12-RR03034NIGMS NIH HHS 1F31GM65793NIGMS NIH HHS F31 GM065793NIGMS NIH HHS S06 GM008248NIGMS NIH HHS S06-GM08248
6 · The paper itself

Abstract

We introduced polypurine tract (PPT) mutations, which we had previously tested in an in vitro assay, into the viral clone NL4-3KFSdelta nef. Each mutant was tested for single-round infectivity and virion production. All of the PPT mutations had an effect on replication; however, mutation of the 5' end appeared to have less of an effect on infectivity than mutation of the 3' end of the PPT sequence. Curiously, a mutation in which the entire PPT sequence was randomized (PPTSUB) retained 12% of the infectivity of the wild type (WT) in a multinuclear activation of galactosidase indicator assay. Supernatants from these infections contained viral particles, as evidenced by the presence of p24 antigen. Two-long terminal repeat (2-LTR) circle junction analysis following PPTSUB infection revealed that the mutant could form a high percentage of normal junctions. Quantification of the 2-LTR circles using real-time PCR revealed that number of 2-LTR circles from cells infected with the PPTSUB mutant was 3.5 logs greater than 2-LTR circles from cells infected with WT virus. To determine whether the progeny virions from a PPTSUB infection could undergo further rounds of replication, we introduced the PPTSUB mutation into a replication-competent virus. Our results show that the mutant virus is able to replicate and that the infectivity of the progeny virions increases with each passage, quickly reverting to a WT PPT sequence. Together, these experiments confirm that the 3' end of the PPT is important for plus-strand priming and that a virus that completely lacks a PPT can replicate at a low level.

Indexed as

MutationBase SequenceCell LineDNA, CircularDNA, ViralHIV-1HIV Long Terminal RepeatHumansVirulenceVirus ReplicationDNA, CircularDNA, Viral

Identifiers

PMID15890925
PMCPMC1112125
OpenAlexW2124974948

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.