The HIV-1 5’ LTR poly(A) site is inactivated by U1 snRNP interaction with the downstream major splice donor site
Open accessAbstract
The inactivity of the 5' long terminal repeat (LTR) poly(A) site immediately downstream of the cap site maximizes the production of HIV-1 transcripts. In this paper, we demonstrate that this inactivity is mediated by the interaction of the U1 snRNP with the major splice donor site (MSD). The inhibition of the HIV-1 poly(A) site by U1 snRNP relies on a series of delicately balanced RNA processing signals. These include the poly(A) site, the major splice donor site and the splice acceptor sites. The inherent efficiency of the HIV-1 poly(A) site allows maximal activity where there is no donor site (in the 3' LTR) but full inhibition by the downstream MSD (in the 5' LTR). The MSD must interact efficiently with U1 snRNP to completely inhibit the 5' LTR poly(A) site, whereas the splice acceptor sites are inefficient, allowing full-length genomic RNA production.
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In both HIV-1 and foamy viruses, the primary factor in splice-site-mediated suppression is the binding of U1 snRNP to the major splice donor site.
“Furthermore, in both HIV-1 and foamy viruses, the primary factor in splice-site-mediated suppression is the binding of U1 small nuclear ribonucleoprotein (U1 snRNP), part of the spliceosome complex, to the major splice donor site (Ashe et al. 1995, 1997, 2000, Schrom et al. 2013).”
From Beyond reverse transcription: molecular mechanisms and emerging paradigms in retroviral replication (2026) · cites this paper as Ashe et al. 1997
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Göttlinger, H. G., Sodroski, J. G., & Haseltine, W. A. (1989) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.86.15.5781 · Cited by 841 · see citing works
Fäcke, M., Janetzko, A., Shoeman, R. L., & Kräusslich, H. G. (1993) · Journal of Virology · doi:10.1128/jvi.67.8.4972-4980.1993 · Cited by 198 · see citing works
Ashe, M. P., Griffin, P., James, W., & Proudfoot, N. J. (1995) · Genes & Development · doi:10.1101/gad.9.23.3008 · Cited by 125 · see citing works
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The transcriptional cycle of HIV-1 in real-time and live cells
Boireau, S., Maiuri, P., Basyuk, E., de la Mata, M., Knezevich, A., Pradet-Balade, B., Bäcker, V., Kornblihtt, A., Marcello, A., & Bertrand, E. (2007) · The Journal of Cell Biology · doi:10.1083/jcb.200706018 · Cited by 191 · see citing works
Schrom, E.-M., Moschall, R., Hartl, M. J., Weitner, H., Fecher, D., Langemeier, J., Bohne, J., Wöhrl, B. M., & Bodem, J. (2013) · Retrovirology · doi:10.1186/1742-4690-10-55 · Cited by 14 · see citing works
Beyond reverse transcription: molecular mechanisms and emerging paradigms in retroviral replication
Jehad, M. A., Ali, L. M., Pillai, V. N., Prabhu, S. G., Mustafa, F., & Rizvi, T. A. (2026) · FEMS Microbiology Reviews · doi:10.1093/femsre/fuaf066 · Cited by 5 · see citing works
“Furthermore, in both HIV-1 and foamy viruses, the primary factor in splice-site-mediated suppression is the binding of U1 small nuclear ribonucleoprotein (U1 snRNP), part of the spliceosome complex, to the major splice donor site (Ashe et al. 1995 , 1997 , 2000 , Schrom et al. 2013 ).”
- Authors
- Ashe, M. P., Pearson, L. H., & Proudfoot, N. J.
- Affiliations
- University of Oxford (GB)
- ORCID
- Ashe, Mark P.
- Venue
- The EMBO Journal
- Published
- 1997-09-15
- Volume
- 16
- Issue
- 18
- Pages
- 5752-5763
- ISSN
- 0261-4189 (ISSN-L)
- 1460-2075
- PMC
- PMC1170206
- OpenAlex
- W2156223412
- Cited by
- 118
- References
- 3
- Citations by year
- 2025: 6 · 2024: 3 · 2023: 7 · 2022: 2 · 2021: 1 · 2020: 3 · 2019: 3 · 2018: 5 · 2017: 2 · 2016: 2 · 2015: 2 · 2014: 4 · 2013: 6 · 2012: 3
- FWCI
- 2.37
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The EMBO Journal (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Research Explorer (The University of Manchester) (submittedVersion)
- Funders
- Wellcome Trust
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Research and Splicing
- Life Sciences › Immunology and Microbiology › Virology › HIV Research and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA and protein synthesis mechanisms
- Keywords
- HIV-1, 5' long terminal repeat, poly(A) site, U1 snRNP, RNA splicing, polyadenylation, RNA processing, splice acceptor site, viral RNA synthesis, cap site
- MeSH terms
- Base Sequence, Globins, HeLa Cells, Humans, Molecular Sequence Data, Poly A, Promoter Regions, Genetic, Recombinant Proteins, RNA Splicing, Transcription, Genetic, Transfection, HIV-1, Mutagenesis, Site-Directed, HIV Long Terminal Repeat, Ribonucleoprotein, U1 Small Nuclear
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