Evidence map›Paper›PMID 23084856›Full record

ArticleJournal of molecular biology2013

Interrelationship between HIV-1 fitness and mutation rate.

Michael J Dapp, Richard H Heineman, Louis M Mansky

Abstract read
In one paragraph

Article in Journal of molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
–field-weighted citation impact
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

27 citing papers in PubMed.

  1. Article
  2. The Evolutionary Interplay of Somatic and Germline Mutation Rates.Annual review of biomedical data science · 2024
    Review
  3. Review
  4. A New HIV-1 KMicrobiology spectrum · 2022
    Article
  5. Article
  6. Intra-Host Diversity of Dengue Virus in Mosquito Vectors.Frontiers in cellular and infection microbiology · 2022
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Quasispecies and virus.European biophysics journal : EBJ · 2018
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
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

3 authors.

Michael J DappInstitute for Molecular Virology, Academic Health Center, University of Minnesota, Minneapolis, MN 55455, USA.
Richard H Heineman
Louis M Mansky

Funding

Training in PharmacoNeuroImmune Substance Abuse ResearchT32DA007097 · NIDA · UNIVERSITY OF MINNESOTA TWIN CITIES · PI MOLITOR, THOMAS WILLIAM · 1985 to 2021
$13.1M
MINNESOTA PAIN RESEARCH TRAINING PROGRAMT32DE007288 · NIDCR · UNIVERSITY OF MINNESOTA TWIN CITIES · PI HERZBERG, MARK C · 1996 to 2011
$8.8M
Mechanisms of HIV-1 VariationR01GM056615 · NIGMS · UNIVERSITY OF MINNESOTA TWIN CITIES · PI MANSKY, LOUIS M. · 2003 to 2011
$2.6M
NIDA NIH HHS T32 DA007097NIDA NIH HHS T32DA007097NIDCR NIH HHS T32 DE007288NIDCR NIH HHS T32DE007288NIGMS NIH HHS R01 GM056615NIGMS NIH HHS R01 GM56615
6 · The paper itself

Abstract

Differences in replication fidelity, as well as mutator and antimutator strains, suggest that virus mutation rates are heritable and prone to natural selection. Human immunodeficiency virus type 1 (HIV-1) has many distinct advantages for the study of mutation rate optimization given the wealth of structural and biochemical data on HIV-1 reverse transcriptase (RT) and mutants. In this study, we conducted parallel analyses of mutation rate and viral fitness. In particular, a panel of 10 RT mutants-most having drug resistance phenotypes-was analyzed for their effects on viral fidelity and fitness. Fidelity differences were measured using single-cycle vector assays, while fitness differences were identified using ex vivo head-to-head competition assays. As anticipated, virus mutants possessing either higher or lower fidelity had a corresponding loss in fitness. While the virus panel was not chosen randomly, it is interesting that it included more viruses possessing a mutator phenotype rather than viruses possessing an antimutator phenotype. These observations provide the first description of an interrelationship between HIV-1 fitness and mutation rate and support the conclusion that mutator and antimutator phenotypes correlate with reduced viral fitness. In addition, the findings here help support a model in which fidelity comes at a cost of replication kinetics and may help explain why retroviruses like HIV-1 and RNA viruses maintain replication fidelity near the extinction threshold.

Indexed as

Mutation RateVirus ReplicationDrug Resistance, ViralHIV-1HIV Reverse TranscriptaseHumansMutationPhenotypeHIV Reverse Transcriptasereverse transcriptase, Human immunodeficiency virus 1

Identifiers

PMID23084856
PMCPMC3534800

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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.