Human p32 protein relieves a post-transcriptional block to HIV replication in murine cells.

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.