Differential Effects of Human Immunodeficiency Virus Type 1 Capsid and Cellular Factors Nucleoporin 153 and LEDGF/p75 on the Efficiency and Specificity of Viral DNA Integration
Open accessAbstract
Retroviruses integrate into cellular DNA nonrandomly. Lentiviruses such as human immunodeficiency virus type 1 (HIV-1) favor the bodies of active genes and gene-enriched transcriptionally active regions of chromosomes. The interaction between lentiviral integrase and the cellular protein lens epithelium-derived growth factor (LEDGF)/p75 underlies the targeting of gene bodies, whereas recent research has highlighted roles for the HIV-1 capsid (CA) protein and cellular factors implicated in viral nuclear import, including transportin 3 (TNPO3) and nucleoporin 358 (NUP358), in the targeting of gene-dense regions of chromosomes. Here, we show that CA mutations, which include the substitution of Asp for Asn74 (N74D), significantly reduce the dependency of HIV-1 on LEDGF/p75 during infection and that this difference correlates with the efficiency of viral DNA integration. The distribution of integration sites mapped by Illumina sequencing confirms that the N74D mutation reduces integration into gene-rich regions of chromosomes and gene bodies and reveals previously unrecognized roles for NUP153 (another HIV-1 cofactor implicated in viral nuclear import) and LEDGF/p75 in the targeting of the viral preintegration complex to gene-dense regions of chromatin. A role for the CA protein in determining the dependency of HIV-1 on LEDGF/p75 during infection highlights a connection between the viral capsid and chromosomal DNA integration.
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Depletion of cellular Nup153 or Nup358 shifts HIV-1 integration away from gene-dense regions of chromatin.
“Depletion of cellular Nup153 or Nup358 also shifted HIV-1 integration away from gene-dense regions of chromatin88,89”
From Structure and function of retroviral integrase (2022) · cites this paper as [88]
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- Authors
- Koh, Y., Wu, X., Ferris, A. L., Matreyek, K. A., Smith, S. J., Lee, K., KewalRamani, V. N., Hughes, S. H., & Engelman, A.
- Affiliations
- Harvard University (US)
- Frederick National Laboratory for Cancer Research (US)
- ORCID
- Venue
- Journal of Virology
- Publisher
- American Society for Microbiology
- Published
- 2013-01
- Volume
- 87
- Issue
- 1
- Pages
- 648-658
- ISSN
- 0022-538X (ISSN-L)
- 1098-5514
- PMC
- PMC3536403
- OpenAlex
- W2010465583
- Cited by
- 122
- References
- 67
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 3 · 2023: 4 · 2022: 5 · 2021: 10 · 2020: 9 · 2019: 9 · 2018: 14 · 2017: 9 · 2016: 17 · 2015: 13 · 2014: 10 · 2013: 12
- FWCI
- 5.00
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Virology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Funders
- National Institutes of Health
- National Cancer Institute
- National Institute of Allergy and Infectious Diseases (AI052014, AI039394, R01AI039394, R37AI039394, R01AI052014)
- Topics
- Life Sciences › Immunology and Microbiology › Virology › HIV Research and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Virus-based gene therapy research
- Health Sciences › Medicine › Infectious Diseases › HIV/AIDS drug development and treatment
- Keywords
- HIV-1, capsid protein, LEDGF/p75, Nup153, viral DNA integration, preintegration complex, integration site mapping, chromatin targeting
- MeSH terms
- Animals, Cell Line, DNA, Viral, Humans, Transcription Factors, HIV-1, Virus Integration, Mutation, Missense, Nuclear Pore Complex Proteins, Capsid Proteins, Adaptor Proteins, Signal Transducing, Mutant Proteins, Mice, Host-Pathogen Interactions
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