The DOI matches its Crossref record; 26 of the 26 references it cites were found in a registry or an index.
Emergence of human immunodeficiency virus type 1 variants with resistance to multiple dideoxynucleosides in patients receiving therapy with dideoxynucleosides.
Open accessAbstract
A set of mutations [Ala-62-->Val(A62V), V75I, F77L, F116Y, and Q151M] in the polymerase domain of reverse transcriptase (RT) of human immunodeficiency virus type 1 (HIV-1) confers on the virus a reduced sensitivity to multiple antiretroviral dideoxynucleosides and has been seen in HIV-1 variants isolated from patients receiving combination chemotherapy with 3'-azido-3'-deoxythymidine (AZT) plus 2',3'-dideoxycytidine (ddC) or 2',3'-dideoxyinosine (ddI). The IC50 values of AZT, ddC, ddI, 2',3'-dideoxyguanosine, and 2',3'-didehydro-3'-deoxythymidine against an infectious clone constructed to include the five mutations were significantly higher than those of a wild-type infectious clone. The K1 value for AZT 5'-triphosphate determined for the virus-associated RT from a posttherapy strain was 35-fold higher than that of RT from a pretherapy strain. Detailed analysis of HIV-1 strains isolated at various times during therapy showed that the Q151M mutation developed first in vivo, at the time when the viremia level suddenly increased, followed by the F116Y and F77L mutations. All five mutations ultimately developed, and the viremia level rose even further. Analyses based on the three-dimensional structure of HIV-1 RT suggest that the positions where at least several of the five mutations occur are located in close proximity to the proposed dNTP-binding site of RT and the first nucleotide position of the single-stranded template.
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Cites
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Multiple Mutations in HIV-1 Reverse Transcriptase Confer High-Level Resistance to Zidovudine (AZT)
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Self-citationInhibition of HIV-1 Replication by a Nonnucleoside Reverse Transcriptase Inhibitor
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Resistance to ddI and Sensitivity to AZT Induced by a Mutation in HIV-1 Reverse Transcriptase
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Endoproteolytic cleavage of gp160 is required for the activation of human immunodeficiency virus
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Characterization of Highly Immunogenic p66/p51 as the Reverse Transcriptase of HTLV-III/LAV
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Cited by
Sarafianos, S. G., Das, K., Clark, A. D., Ding, J., Boyer, P. L., Hughes, S. H., & Arnold, E. (1999) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.96.18.10027 · Cited by 309
Self-citationMolecular mechanisms of HIV-1 resistance to nucleoside reverse transcriptase inhibitors (NRTIs)
Sluis-Cremer, N., Arion, D., & Parniak*, M. A. (2000) · Cellular and Molecular Life Sciences · doi:10.1007/pl00000626 · Cited by 117
Avoiding drug resistance in HIV reverse transcriptase
Cilento, M. E., Kirby, K. A., & Sarafianos, S. G. (2021) · Chemical Reviews · doi:10.1021/acs.chemrev.0c00967 · Cited by 106
Metadata
- Authors
- Shirasaka, T., Kavlick, M. F., Ueno, T., Gao, W. Y., Kojima, E., Alcaide, M. L., Chokekijchai, S., Roy, B. M., Arnold, E., & Yarchoan, R.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1995-03-14
- Volume
- 92
- Issue
- 6
- Pages
- 2398-2402
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2008428638
- Cited by
- 386
- References
- 26
- FWCI
- 19.73
- Type
- journal article
- Language
- en
- Open access
- green
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- Shirasaka, T., Kavlick, M. F., Ueno, T., Gao, W. Y., Kojima, E., Alcaide, M. L., Chokekijchai, S., Roy, B. M., Arnold, E., & Yarchoan, R. (1995). Emergence of human immunodeficiency virus type 1 variants with resistance to multiple dideoxynucleosides in patients receiving therapy with dideoxynucleosides. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.92.6.2398
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