ArticleRetrovirology2017
HIV-1 tolerates changes in A-count in a small segment of the pol gene.
Article in Retrovirology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Insights into Synonymous Codon Usage Bias in Hepatitis C Virus and Its Adaptation to Hosts.Pathogens (Basel, Switzerland) · 2023Article
- Silent codon positions in the A-rich HIV RNA genome that do not easily become A: Restrictions imposed by the RNA sequence and structure.Virus evolution · 2022Article
- The HIV 5' Gag Region Displays a Specific Nucleotide Bias Regulating Viral Splicing and Infectivity.Viruses · 2021Article
- Impact of Synonymous Genome Recoding on the HIV Life Cycle.Frontiers in microbiology · 2021Review
- New windows into retroviral RNA structures.Retrovirology · 2018Review
- RNA Structure-A Neglected Puppet Master for the Evolution of Virus and Host Immunity.Frontiers in immunology · 2018Review
- Increasing the CpG dinucleotide abundance in the HIV-1 genomic RNA inhibits viral replication.Retrovirology · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe HIV-1 RNA genome has a biased nucleotide composition with a surplus of As. Several hypotheses have been put forward to explain this striking phenomenon, but the A-count of the HIV-1 genome has thus far not been systematically manipulated. The reason for this reservation is the likelihood that known and unknown sequence motifs will be affected by such a massive mutational approach, thus resulting in replication-impaired virus mutants. We present the first attempt to increase and decrease the A-count in a relatively small polymerase (pol) gene segment of HIV-1 RNA.
resultsTo minimize the mutational impact, a new mutational approach was developed that is inspired by natural sequence variation as present in HIV-1 isolates. This phylogeny-instructed mutagenesis allowed us to create replication-competent HIV-1 mutants with a significantly increased or decreased local A-count. The local A-count of the wild-type (wt) virus (40.2%) was further increased to 46.9% or reduced to 31.7 and 26.3%. These HIV-1 variants replicate efficiently in vitro, despite the fact that the pol changes cause a quite profound move in HIV-SIV sequence space.
conclusionsExtrapolating these results to the complete 9 kb RNA genome, we may cautiously suggest that the A-rich signature does not have to be maintained. This survey also provided clues that silent codon changes, in particular from G-to-A, determine the subtype-specific sequence signatures.
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