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Paracrine Signals from HIV-1 Infected Immune Cells Reprogram Cervical Cancer Pathways.

Charles Ochieng' Olwal1,2, Ujjwal Rathore3,4, Sara Makanani5,6,7

  • 1West African Centre for Cell Biology of Infectious Pathogens (WACCBIP), College of Basic and Applied Sciences, University of Ghana, Accra, Ghana.

Biorxiv : the Preprint Server for Biology
|July 15, 2025
PubMed
Summary

Human papillomavirus (HPV) causes cervical cancer. Women with HPV and human immunodeficiency virus type 1 (HIV-1) have higher cancer risk, as HIV-1 alters cervical cell signaling pathways, suggesting PI3K pathway as a therapeutic target.

Keywords:
HPV-associated cervical cancerHPV/HIV coinfectionMAPK and PI3K signalingNetwork propagation

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A Proximal Culture Method to Study Paracrine Signaling Between Cells
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Area of Science:

  • Oncology
  • Virology
  • Immunology

Background:

  • Persistent human papillomavirus (HPV) infection is the primary cause of cervical cancer.
  • Co-infection with HPV and human immunodeficiency virus type 1 (HIV-1) significantly increases cervical cancer risk, even with treatment.
  • The mechanisms by which HIV-1 influences cervical cell signaling remain unclear.

Purpose of the Study:

  • To investigate how HIV-1 infection alters signaling pathways in cervical cells.
  • To identify molecular mechanisms linking HIV-1 and increased cervical cancer risk.
  • To explore potential therapeutic targets for HIV-associated cervical cancer.

Main Methods:

  • Global transcriptomics analysis of cervical swabs from Kenyan women stratified by HPV, HIV-1, and cancer status.
  • Global mass spectrometry (MS) proteomics of cervical cells exposed to HIV-1-infected CD4+ T-cell secretome.
  • Integrative network analyses of transcriptomic and proteomic data.
  • Phosphoproteomics MS analysis to confirm pathway activation.

Main Results:

  • HIV-1 infected women exhibited cancer-like gene expression patterns in non-cancerous cervical epithelial cells.
  • Proteomic analysis revealed altered MAPK, PI3K-AKT, and β-catenin signaling pathways.
  • IRS-1 and interferon-stimulated genes were upregulated in both patient samples and cell cultures.
  • PI3K-AKT pathway activation was confirmed in cervical cells exposed to HIV-1-infected T-cell media.

Conclusions:

  • HIV-1 infection reshapes cervical cell signaling through paracrine mechanisms.
  • The PI3K-AKT pathway is a key mediator of HIV-1's effect on cervical cells.
  • Targeting the PI3K pathway may offer a novel therapeutic strategy for HIV-associated cervical cancer.