期刊
JOURNAL OF VIROLOGY
卷 78, 期 4, 页码 2082-2087出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.78.4.2082-2087.2004
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资金
- NCI NIH HHS [CA5077] Funding Source: Medline
- NIAID NIH HHS [AI51910, AI43886, R41 AI051910, R42 AI051910] Funding Source: Medline
Human immunodeficiency virus type 1 (HIV-1) utilizes a distinctive form of gene regulation as part of its life cycle, termed programmed -1 ribosomal frameshifting, to produce the required ratio of the Gag and Gag-Pol polyproteins. We carried out a sequence comparison of 1,000 HIV-1 sequences at the slippery site (UUUUUUA) and found that the site is invariant, which is somewhat surprising for a virus known for its variability. This prompted us to prepare a series of mutations to examine their effect upon frameshifting and viral infectivity. Among the series of mutations were changes of the HIV-1 slippery site to those effectively utilized by other viruses, because such mutations would be anticipated to have a relatively mild effect upon frameshifting. The results demonstrate that any change to the slippery site reduced frameshifting levels and also dramatically inhibited infectivity. Because ribosomal frameshifting is essential for HIV-1 replication and it is surprisingly resistant to mutation, modulation of HIV-1 frameshifting efficiency potentially represents an important target for the development of novel antiviral therapeutics.
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