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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.

Original publication




Journal article



Publication Date





5752 - 5763


Base Sequence, Globins, HIV Long Terminal Repeat, HIV-1, HeLa Cells, Humans, Molecular Sequence Data, Mutagenesis, Site-Directed, Poly A, Promoter Regions, Genetic, RNA Splicing, Recombinant Proteins, Ribonucleoprotein, U1 Small Nuclear, Transcription, Genetic, Transfection