ArticleRetrovirology2013
DNA damage enhances integration of HIV-1 into macrophages by overcoming integrase inhibition.
Article in Retrovirology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- microRNA-422a promotes HIV replication and innate immune evasion by targeting MECP2.Molecular therapy. Nucleic acids · 2026Article
- Topoisomerase Inhibitors Increase Episomal DNA Expression by Inducing the Integration of Episomal DNA in Hepatic Cells.Pharmaceutics · 2023Article
- Lentiviral Vectors for Ocular Gene Therapy.Pharmaceutics · 2022Review
- Identification of an integrase-independent pathway of retrotransposition.Science advances · 2022Article
- Viral Modulation of the DNA Damage Response and Innate Immunity: Two Sides of the Same Coin.Journal of molecular biology · 2022Review
- Borna disease virus docks on neuronal DNA double-strand breaks to replicate and dampens neuronal activity.iScience · 2022Article
- Improved Functionality of Integration-Deficient Lentiviral Vectors (IDLVs) by the Inclusion of ISPharmaceutics · 2021Article
- HIV-1 Tat protein induces DNA damage in human peripheral blood B-lymphocytes via mitochondrial ROS production.Redox biology · 2018Article
- Structural alteration of DNA induced by viral protein R of HIV-1 triggers the DNA damage response.Retrovirology · 2018Article
- DNA damage induced by topoisomerase inhibitors activates SAMHD1 and blocks HIV-1 infection of macrophages.The EMBO journal · 2018Article
- IDLV-HIV-1 Env vaccination in non-human primates induces affinity maturation of antigen-specific memory B cells.Communications biology · 2018Article
- Imaging HIV-1 Genomic DNA from Entry through Productive Infection.Journal of virology · 2017Article
- An Overview of Human Immunodeficiency Virus Type 1-Associated Common Neurological Complications: Does Aging Pose a Challenge?Journal of Alzheimer's disease : JAD · 2017Review
- Differences in vector-genome processing and illegitimate integration of non-integrating lentiviral vectors.Gene therapy · 2017Article
- Article
- Poly(ADP-ribose) polymerase-1 silences retroviruses independently of viral DNA integration or heterochromatin formation.The Journal of general virology · 2016Article
- Insight into the ERVK Integrase - Propensity for DNA Damage.Frontiers in microbiology · 2016Article
- MARCH8 inhibits HIV-1 infection by reducing virion incorporation of envelope glycoproteins.Nature medicine · 2015Article
- Therapeutic doses of irradiation activate viral transcription and induce apoptosis in HIV-1 infected cells.Virology · 2015Article
- BRCA1 functions as a novel transcriptional cofactor in HIV-1 infection.Virology journal · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe prevention of persistent human immunodeficiency virus type 1 (HIV-1) infection requires the clarification of the mode of viral transduction into resting macrophages. Recently, DNA double-strand breaks (DSBs) were shown to enhance infection by D64A virus, which has a defective integrase catalytic activity (IN-CA). However, the mechanism by which DSBs upregulate viral transduction was unclear. Here we analyzed the roles of DSBs during IN-CA-independent viral transduction into macrophages.
resultsWe used cellular systems with rare-cutting endonucleases and found that D64A virus integrated efficiently into the sites of artificially induced DSBs. This IN-CA-independent viral transduction was blocked by an inhibitor of ataxia telangiectasia mutated protein (ATM) but was resistant to raltegravir (RAL), an inhibitor of integrase activity during strand transfer. Moreover, Vpr, an accessory gene product of HIV-1, induced DSBs in resting macrophages and significantly enhanced the rate of IN-CA-independent viral transduction into macrophages with concomitant production of secondary viruses.
conclusionDSBs contribute to the IN-CA-independent viral infection of macrophages, which is resistant to RAL. Thus, the ATM-dependent cellular pathway and Vpr-induced DNA damage are novel targets for preventing persistent HIV-1 infection.
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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.