Abstract
In the mouse, replication of human immunodeficiency virus type 1 (HIV) is blocked at the levels of entry, transcription and assembly. For the latter effect, the amounts of unspliced viral genomic RNA could have an important function. Indeed, in murine cells, HIV transcripts are spliced excessively, a process that is not inhibited by the murine splicing inhibitor p32 (mp32). In marked contrast, its human counterpart, hp32, not only blocks this splicing but promotes the accumulation of viral genomic transcripts and structural proteins, resulting in the assembly and release of infectious virions. A single substitution in hp32 of Gly 35 to Asp 35, which is found in mp32, abrogates this activity. Thus, hp32 overcomes an important post-transcriptional block to HIV replication in murine cells.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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3T3 Cells
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Amino Acid Sequence / genetics
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Animals
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Aspartic Acid / genetics
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Carrier Proteins
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Gene Products, rev / genetics
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Glycine / genetics
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HIV / genetics*
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HIV / metabolism
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HIV Infections / genetics*
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Humans
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Mice
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Mitochondrial Proteins
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Nuclear Proteins / genetics*
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Point Mutation / genetics
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RNA Processing, Post-Transcriptional / genetics
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RNA Splicing / genetics*
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RNA, Viral / genetics*
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RNA-Binding Proteins
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Serine-Arginine Splicing Factors
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Up-Regulation / genetics
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Virus Replication / genetics*
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rev Gene Products, Human Immunodeficiency Virus
Substances
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C1QBP protein, human
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Carrier Proteins
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Gene Products, rev
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Mitochondrial Proteins
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Nuclear Proteins
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RNA, Viral
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RNA-Binding Proteins
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rev Gene Products, Human Immunodeficiency Virus
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Serine-Arginine Splicing Factors
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Aspartic Acid
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Glycine