ArticleRetrovirology2011
Residual HIV-1 DNA Flap-independent nuclear import of cPPT/CTS double mutant viruses does not support spreading infection.
Article in Retrovirology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Adaptation of lentiviral vectors for viral gene therapy and their impact on host cell biology.Journal of translational medicine · 2026Review
- Structure-specific nucleases in genome dynamics and strategies for targeting cancers.Journal of molecular cell biology · 2024Review
- HIV Reservoir: How to Measure It?Current HIV/AIDS reports · 2023Review
- Review
- HIV-based lentiviral vectors: origin and sequence differences.Molecular therapy. Methods & clinical development · 2021Article
- Avoiding Drug Resistance in HIV Reverse Transcriptase.Chemical reviews · 2021Review
- Factors that mold the nuclear landscape of HIV-1 integration.Nucleic acids research · 2021Review
- Measuring the subcellular compartmentalization of viral infections by protein complementation assay.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Microtubule-associated proteins 1 (MAP1) promote human immunodeficiency virus type I (HIV-1) intracytoplasmic routing to the nucleus.The Journal of biological chemistry · 2015Article
- SiRNA-induced mutation in HIV-1 polypurine tract region and its influence on viral fitness.PloS one · 2015Article
- Nuclear import of APOBEC3F-labeled HIV-1 preintegration complexes.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Quantitative analysis of the time-course of viral DNA forms during the HIV-1 life cycle.Retrovirology · 2013Article
- The importance of becoming double-stranded: Innate immunity and the kinetic model of HIV-1 central plus strand synthesis.Virology · 2013Review
- The HIV-1 passage from cytoplasm to nucleus: the process involving a complex exchange between the components of HIV-1 and cellular machinery to access nucleus and successful integration.International journal of biochemistry and molecular biology · 2012Article
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Authors and funding
8 authors.
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No grant is acknowledged in the PubMed record.
Abstract
unlabelled
backgroundThe human immunodeficiency virus type 1 (HIV-1) central DNA Flap is generated during reverse transcription as a result of (+) strand initiation at the central polypurine tract (cPPT) and termination after a ca. 100 bp strand displacement at the central termination sequence (CTS). The central DNA Flap is a determinant of HIV-1 nuclear import, however, neither cPPT nor CTS mutations entirely abolish nuclear import and infection. Therefore, to determine whether or not the DNA Flap is essential for HIV-1 nuclear import, we generated double mutant (DM) viruses, combining cPPT and CTS mutations to abolish DNA Flap formation.
resultsThe combination of cPPT and CTS mutations reduced the proportion of viruses forming the central DNA Flap at the end of reverse transcription and further decreased virus infectivity in one-cycle titration assays. The most affected DM viruses were unable to establish a spreading infection in the highly permissive MT4 cell line, nor in human primary peripheral blood mononuclear cells (PBMCs), indicating that the DNA Flap is required for virus replication. Surprisingly, we found that DM viruses still maintained residual nuclear import levels, amounting to 5-15% of wild-type virus, as assessed by viral DNA circle quantification. Alu-PCR quantification of integrated viral genome also indicated 5-10% residual integration levels compared to wild-type virus.
conclusionThis work establishes that the central DNA Flap is required for HIV-1 spreading infection but points to a residual DNA Flap independent nuclear import, whose functional significance remains unclear since it is not sufficient to support viral replication.
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