ArticleJournal of virology1996
Retroviral mutation rates and A-to-G hypermutations during different stages of retroviral replication.
Article in Journal of virology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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.
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.
Who cites it
30 citing papers in PubMed, 79 citations in OpenAlex.
- Review
- Molecular Biology and Diversification of Human Retroviruses.Frontiers in virology (Lausanne, Switzerland) · 2022Article
- Development of a User-Friendly Pipeline for Mutational Analyses of HIV Using Ultra-Accurate Maximum-Depth Sequencing.Viruses · 2021Article
- The Determination of HIV-1 RT Mutation Rate, Its Possible Allosteric Effects, and Its Implications on Drug Resistance.Viruses · 2020Review
- Development of Lentiviral Vectors for HIV-1 Gene Therapy with Vif-Resistant APOBEC3G.Molecular therapy. Nucleic acids · 2019Article
- APOBEC3G Regulation of the Evolutionary Race Between Adaptive Immunity and Viral Immune Escape Is Deeply Imprinted in the HIV Genome.Frontiers in immunology · 2018Article
- Hepatitis C virus: Promising discoveries and new treatments.World journal of gastroenterology · 2016Review
- Minimal Contribution of APOBEC3-Induced G-to-A Hypermutation to HIV-1 Recombination and Genetic Variation.PLoS pathogens · 2016Article
- Hepatitis C virus genetic variability and evolution.World journal of hepatology · 2015Review
- Review
- Endogenous retrovirus induces leukemia in a xenograft mouse model for primary myelofibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Variation in RNA virus mutation rates across host cells.PLoS pathogens · 2014Article
- HIV-1 reverse transcription.Cold Spring Harbor perspectives in medicine · 2012Review
- Retrovolution: HIV-driven evolution of cellular genes and improvement of anticancer drug activation.PLoS genetics · 2012Article
- Nature, position, and frequency of mutations made in a single cycle of HIV-1 replication.Journal of virology · 2010Article
- Article
- Avian myeoloblastosis virus (AMV): only one side of the coin.Retrovirology · 2008Review
- Mutations in the RNase H primer grip domain of murine leukemia virus reverse transcriptase decrease efficiency and accuracy of plus-strand DNA transfer.Journal of virology · 2005Article
- Unselected mutations in the human immunodeficiency virus type 1 genome are mostly nonsynonymous and often deleterious.Journal of virology · 2004Article
- Genetic variability: the key problem in the prevention and therapy of RNA-based virus infections.Medicinal research reviews · 2003Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Retroviruses mutate at a high rate in vivo during viral replication. Mutations may occur during proviral transcription by RNA polymerase II, during minus-strand DNA synthesis (RNA template) by viral reverse transcriptase, or during plus-strand DNA synthesis (DNA template) by reverse transcriptase. To determine the contributions of different stages of replication to the retroviral mutation rates, we developed a spleen necrosis virus-based in vivo system to selectively identify mutations occurring during the early stage (RNA transcription plus minus-strand synthesis) and the late stage (plus-strand synthesis plus DNA repair). A lacZalpha reporter gene was inserted into the long terminal repeat (LTR) of a spleen necrosis virus shuttle vector, and proviruses were recovered from infected cells as plasmids containing either one or both LTRs. Plasmids containing both LTRs generated a mutant phenotype only if the lacZalpha genes in both LTRs were mutated, which is most likely to occur during the early stage. Mutant phenotypes were identified from plasmids containing one LTR regardless of the stage at which the mutations occurred. Thus, mutant frequencies obtained after recovery of plasmids containing both LTRs or one LTR provided early-stage and total mutation rates, respectively. Analysis of 56,409 proviruses suggested that the retroviral mutation rates during the early and late stages of replication were equal or within twofold of each other. In addition, two mutants with A-to-G hypermutations were discovered, suggesting a role for mammalian double-stranded RNA adenosine deaminase enzyme in retroviral mutations. These experiments provide a system to selectively identify mutations in the early stage of retroviral replication and to provide upper and lower limits to the in vivo mutation rates during minus-strand and plus-strand synthesis, respectively.
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What OpenQuestion holds
Registered trials
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.