ArticlePloS one2014
Repair of oxidative DNA base damage in the host genome influences the HIV integration site sequence preference.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Genotoxic consequences of viral infections.Npj viruses · 2025Review
- DNA strand breaks and gaps target retroviral intasome binding and integration.Nature communications · 2023Article
- OGG1 inhibition suppresses African swine fever virus replication.Virologica Sinica · 2023Article
- Both ATM and DNA-PK Are the Main Regulators of HIV-1 Post-Integrational DNA Repair.International journal of molecular sciences · 2023Article
- Association ofFrontiers in genetics · 2022Article
- Strategies for Targeting Retroviral Integration for Safer Gene Therapy: Advances and Challenges.Frontiers in molecular biosciences · 2021Review
- NHEJ pathway is involved in post-integrational DNA repair due to Ku70 binding to HIV-1 integrase.Retrovirology · 2019Article
- A CRISPR/Cas9 approach reveals that the polymerase activity of DNA polymerase β is dispensable for HIV-1 infection in dividing and nondividing cells.The Journal of biological chemistry · 2017Article
- Removal of nuclease contamination during purification of recombinant prototype foamy virus integrase.Journal of virological methods · 2016Article
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Authors and funding
8 authors.
Funding
Abstract
Host base excision repair (BER) proteins that repair oxidative damage enhance HIV infection. These proteins include the oxidative DNA damage glycosylases 8-oxo-guanine DNA glycosylase (OGG1) and mutY homolog (MYH) as well as DNA polymerase beta (Polβ). While deletion of oxidative BER genes leads to decreased HIV infection and integration efficiency, the mechanism remains unknown. One hypothesis is that BER proteins repair the DNA gapped integration intermediate. An alternative hypothesis considers that the most common oxidative DNA base damages occur on guanines. The subtle consensus sequence preference at HIV integration sites includes multiple G:C base pairs surrounding the points of joining. These observations suggest a role for oxidative BER during integration targeting at the nucleotide level. We examined the hypothesis that BER repairs a gapped integration intermediate by measuring HIV infection efficiency in Polβ null cell lines complemented with active site point mutants of Polβ. A DNA synthesis defective mutant, but not a 5'dRP lyase mutant, rescued HIV infection efficiency to wild type levels; this suggested Polβ DNA synthesis activity is not necessary while 5'dRP lyase activity is required for efficient HIV infection. An alternate hypothesis that BER events in the host genome influence HIV integration site selection was examined by sequencing integration sites in OGG1 and MYH null cells. In the absence of these 8-oxo-guanine specific glycosylases the chromatin elements of HIV integration site selection remain the same as in wild type cells. However, the HIV integration site sequence preference at G:C base pairs is altered at several positions in OGG1 and MYH null cells. Inefficient HIV infection in the absence of oxidative BER proteins does not appear related to repair of the gapped integration intermediate; instead oxidative damage repair may participate in HIV integration site preference at the sequence level.
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