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The gene expression in cells is regulated at different stages: (i) transcription, (ii) RNA processing, (iii) RNA localization, and (iv) translation. Transcriptional regulation is mediated by regulatory proteins such as transcription factors, activators, or repressors—these control gene expression by initiating or inhibiting the transcription of genes. Once a precursor or pre-mRNA is produced, it undergoes post-transcriptional modification, including 5' capping, splicing, and the...
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HIV-1 Infection Regulates Gene Expression by Altering Alternative Polyadenylation Through CPSF6 and CPSF5

Charlotte Luchsinger1, Annie Zhi Dai1, Hari Yalamanchili2

  • 1Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.

Biorxiv : the Preprint Server for Biology
|August 19, 2025
PubMed
Summary

HIV-1 infection causes key proteins (CPSF5 and CPSF6) to move within cells, altering gene expression through alternative polyadenylation (APA). This viral hijacking of cellular processes drives disease.

Keywords:
CPSF5CPSF6HIV-1alternative polyadenylation(APA)capsidgene expression

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Area of Science:

  • Molecular Biology
  • Virology
  • Gene Regulation

Background:

  • HIV-1 infection involves nuclear transport of the viral core.
  • Cleavage and polyadenylation specificity factor (CPSF)5 and CPSF6 are involved in alternative polyadenylation (APA).
  • APA regulates mRNA 3'-untranslated regions (3'-UTRs), impacting gene expression.

Purpose of the Study:

  • To investigate if HIV-1 infection-induced changes in CPSF5 and CPSF6 localization alter cellular function.
  • To determine the role of CPSF6-viral capsid interaction in HIV-1-mediated APA regulation.

Main Methods:

  • Assessment of APA in human primary CD4+ T cells and cell lines using two independent methodologies.
  • Analysis of CPSF5 and CPSF6 subcellular localization.
  • Investigation of the interaction between CPSF6 and the HIV-1 viral capsid.

Main Results:

  • HIV-1 infection induces translocation of CPSF5 and CPSF6 to nuclear speckles.
  • HIV-1 infection regulates APA in a manner dependent on CPSF6 interaction with the viral capsid.
  • The observed APA changes mimic those in CPSF6 knockout cells.

Conclusions:

  • HIV-1 infection co-opts CPSF5 and CPSF6 to alter cellular gene expression through APA.
  • The interaction between the HIV-1 capsid and CPSF6 is crucial for manipulating host cell processes.
  • This hijacking of cellular machinery contributes to HIV-1 pathogenesis.