We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
RPLP1 restricts HIV-1 transcription by disrupting C/EBPβ binding to the LTR.
- Authors
Yang, Weijing; Wang, Hong; Li, Zhaolong; Zhang, Lihua; Liu, Jianhui; Kirchhoff, Frank; Huan, Chen; Zhang, Wenyan
- Abstract
Long-term non-progressors (LTNPs) of HIV-1 infection may provide important insights into mechanisms involved in viral control and pathogenesis. Here, our results suggest that the ribosomal protein lateral stalk subunit P1 (RPLP1) is expressed at higher levels in LTNPs compared to regular progressors (RPs). Functionally, RPLP1 inhibits transcription of clade B HIV-1 strains by occupying the C/EBPβ binding sites in the viral long terminal repeat (LTR). This interaction requires the α-helixes 2 and 4 domains of RPLP1 and is evaded by HIV-1 group M subtype C and group N, O and P strains that do not require C/EBPβ for transcription. We further demonstrate that HIV-1-induced translocation of RPLP1 from the cytoplasm to the nucleus is essential for antiviral activity. Finally, knock-down of RPLP1 promotes reactivation of latent HIV-1 proviruses. Thus, RPLP1 may play a role in the maintenance of HIV-1 latency and resistance to RPLP1 restriction may contribute to the effective spread of clade C HIV-1 strains. Here, employing proteomics profiling, the authors identify RPLP1 to be highly expressed in long-term non-progressors of HIV-1 infection. Functional validation shows that RPLP1 inhibits transcription of HIV-1 group M subtype B strains by blocking C/EBPβ binding sites, while RPLP1 knock-down promotes HIV-1 reactivation.
- Subjects
HIV; LONG-term non-progressors; RIBOSOMAL proteins; RIBOSOMES; BINDING sites; CYTOPLASM
- Publication
Nature Communications, 2024, Vol 15, Issue 1, p1
- ISSN
2041-1723
- Publication type
Article
- DOI
10.1038/s41467-024-49622-1