Evidence map›Paper›PMID 11000222›Full record

ArticleJournal of virology2000

In vivo analysis of human T-cell leukemia virus type 1 reverse transcription accuracy.

L M Mansky

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

37 citing papers in PubMed, 79 citations in OpenAlex.

  1. Review
  2. Review
  3. Molecular Biology and Diversification of Human Retroviruses.Frontiers in virology (Lausanne, Switzerland) · 2022
    Article
  4. Article
  5. Novel and emerging mutations of SARS-CoV-2: Biomedical implications.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021
    Review
  6. Article
  7. Article
  8. Review
  9. Evaluation of haplotype callers for next-generation sequencing of viruses.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2020
    Article
  10. Article
  11. Review
  12. Article
  13. Role of Exosomes in Human Retroviral Mediated Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2018
    Review
  14. Article
  15. Mechanisms of viral mutation.Cellular and molecular life sciences : CMLS · 2016
    Review
  16. Review
  17. Review
  18. Review
  19. Review
  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

1 author at 1 institution in 1 country.

L M ManskyDepartment of Molecular Virology, Immunology, and Medical Genetics, The Arthur James Cancer Hospital and Solove Research Institute, Ohio State University Medical Center, Columbus 43210, USA. mansky.3@osu.edu
The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute · US

Funding

Mechanisms of HIV-1 VariationR01GM056615 · NIGMS · UNIVERSITY OF MINNESOTA TWIN CITIES · PI MANSKY, LOUIS M. · 2003 to 2011
$2.6M
MECHANISMS OF HIV1 VARIATIONR29GM056615 · NIGMS · OHIO STATE UNIVERSITY · PI MANSKY, LOUIS M · 1997 to 2001
$215k
NIGMS NIH HHS GM56615NIGMS NIH HHS R01 GM056615NIGMS NIH HHS R29 GM056615
6 · The paper itself

Abstract

Several studies have indicated that the genetic diversity of human T-cell leukemia virus type 1 (HTLV-1), a virus associated with adult T-cell leukemia, is significantly lower than that of other retroviruses, including that of human immunodeficiency virus type 1 (HIV-1). To test whether HTLV-1 variation is lower than other retroviruses, a tractable vector system has been developed to measure reverse transcription accuracy in one round of HTLV-1 replication. This system consists of a HTLV-1 vector that contains a cassette with the neomycin phosphotransferase (neo) gene, a bacterial origin of DNA replication, and the lacZalpha peptide gene region (the mutational target). The vector was replicated by trans-complementation with helper plasmids. The in vivo mutation rate for HTLV-1 was determined to be 7 x 10(-6) mutations per target base pair per replication cycle. The majority of the mutations identified were base substitution mutations, namely, G-to-A and C-to-T transitions, frameshift mutations, and deletion mutations. Mutation of the methionine residue in the conserved YMDD motif of the HTLV-1 reverse transcriptase to either alanine or valine (i.e., M188A or M188V) led to a factor of two increase in the rate of mutation, indicating the role of this motif in enzyme accuracy. The HTLV-1 in vivo mutation rate is comparable to that of bovine leukemia virus (BLV), another member of the HTLV/BLV genus of retroviruses, and is about fourfold lower than that of HIV-1. These observations indicate that while the mutation rate of HTLV-1 is significantly lower than HIV-1, this lower rate alone would not explain the low diversity in HTLV-1 isolates, supporting the hypothesis that HTLV-1 replicates primarily as a provirus during cellular DNA replication rather than as a virus via reverse transcription.

Indexed as

Transcription, GeneticBase SequenceDNA ReplicationHuman T-lymphotropic virus 1Molecular Sequence DataMutationRNA-Directed DNA PolymeraseVirus ReplicationRNA-Directed DNA Polymerase

Identifiers

PMID11000222
PMCPMC112382
OpenAlexW2114577265

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.