SRSF1 RNA recognition motifs are strong inhibitors of HIV-1 replication

Sean Paz, Michael L. Lu, Hiroshi Takata, Lydie Trautmann, Massimo Caputi

Research output: Contribution to journalArticlepeer-review

9 Scopus citations

Abstract

Replication of the integrated HIV-1 genome is tightly regulated by a series of cellular factors. In previous work we showed that transactivation of the HIV-1 promoter is regulated by the cellular splicing factor SRSF1. Here we report that SRSF1 can downregulate the replication of B, C, and D subtype viruses by >200-fold in a cell culture system. We show that viral transcription and splicing are inhibited by SRSF1 expression. Furthermore, SRSF1 deletion mutants containing the protein RNA-binding domains but not the arginine serine-rich activator domain can downregulate viral replication by >2,000-fold with minimal impact on cell viability and apoptosis. These data suggest a therapeutic potential for SRSF1 and its RNA-binding domains.

Original languageEnglish (US)
Pages (from-to)6275-6286
Number of pages12
JournalJournal of virology
Volume89
Issue number12
DOIs
StatePublished - 2015
Externally publishedYes

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Insect Science
  • Virology

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