ArticleRetrovirology2019
NHEJ pathway is involved in post-integrational DNA repair due to Ku70 binding to HIV-1 integrase.
Article in Retrovirology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- New Cellular Partners of HIV-1 Integrase and their Role in Viral Replication.Doklady. Biochemistry and biophysics · 2025Article
- Genotoxic consequences of viral infections.Npj viruses · 2025Review
- Involvement of Human Cellular Proteins and Structures in Realization of the HIV Life Cycle: A Comprehensive Review, 2024.Viruses · 2024Review
- Review
- Brief Histories of Retroviral Integration Research and Associated International Conferences.Viruses · 2024Review
- KuINins as a New Class of HIV-1 Inhibitors That Block Post-Integration DNA Repair.International journal of molecular sciences · 2023Article
- Inhibition of ATM-directed antiviral responses by HIV-1 Vif.PLoS pathogens · 2023Article
- Both ATM and DNA-PK Are the Main Regulators of HIV-1 Post-Integrational DNA Repair.International journal of molecular sciences · 2023Article
- Complex Relationships between HIV-1 Integrase and Its Cellular Partners.International journal of molecular sciences · 2022Review
- Multimodal Functionalities of HIV-1 Integrase.Viruses · 2022Review
- Complex of HIV-1 Integrase with Cellular Ku Protein: Interaction Interface and Search for Inhibitors.International journal of molecular sciences · 2022Article
- Structure and function of retroviral integrase.Nature reviews. Microbiology · 2022Review
- Association of Polymorphisms in NHEJ Pathway Genes with HIV-1 Infection and AIDS Progression in a Northern Chinese MSM Population.Disease markers · 2022Article
- Lactate Suppresses Retroviral Transduction in Cervical Epithelial Cells through DNA-PKcs Modulation.International journal of molecular sciences · 2021Article
- Transcriptome dataset of HEK293T cells depleted of one of the subunits of the DNA-PK complex: Ku70, Ku80 or DNA-PKcs.Data in brief · 2021Article
- Noncytotoxic functions of killer cell granzymes in viral infections.PLoS pathogens · 2021Review
- Evaluation of Epigenetic and Radiomodifying Effects during Radiotherapy Treatments in Zebrafish.International journal of molecular sciences · 2021Review
- Cytoplasmic-translocated Ku70 senses intracellular DNA and mediates interferon-lambda1 induction.Immunology · 2021Article
- SAP domain forms a flexible part of DNA aperture in Ku70/80.The FEBS journal · 2021Article
- The Role of Ku70 as a Cytosolic DNA Sensor in Innate Immunity and Beyond.Frontiers in cellular and infection microbiology · 2021Review
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHIV-1 integration results in genomic DNA gaps that are repaired by cellular DNA repair pathways. This step of the lentiviral life cycle remains poorly understood despite its crucial importance for successful replication. We and others reported that Ku70 protein of the non-homologous end joining pathway (NHEJ) directly binds HIV-1 integrase (IN). Here, we studied the importance of this interaction for post-integrational gap repair and the recruitment of NHEJ factors in this process.
resultsWe engineered HIV-based pseudovirus with mutant IN defective in Ku70 binding and generated heterozygous Ku70, Ku80 and DNA-PKcs human knockout (KO) cells using CRISPR/Cas9. KO of either of these proteins or inhibition of DNA-PKcs catalytic activity substantially decreased the infectivity of HIV-1 with native IN but not with the mutant one. We used a recently developed qPCR assay for the measurement of gap repair efficiency to show that HIV-1 with mutant IN was defective in DNA post-integrational repair, whereas the wild type virus displayed such a defect only when NHEJ system was disrupted in any way. This effect was present in CRISPR/Cas9 modified 293T cells, in Jurkat and CEM lymphoid lines and in primary human PBMCs.
conclusionsOur data provide evidence that IN recruits DNA-PK to the site of HIV-1 post-integrational repair due to Ku70 binding-a novel finding that explains the involvement of DNA-PK despite the absence of free double stranded DNA breaks. In addition, our data clearly indicate the importance of interactions between HIV-1 IN and Ku70 in HIV-1 replication at the post-integrational repair step.
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