Regulation of Autophagy in Cells Infected With Oncogenic Human Viruses and Its Impact on Cancer Development

Research output: Contribution to journalReview articlepeer-review

Abstract

About 20% of total cancer cases are associated to infections. To date, seven human viruses have been directly linked to cancer development: high-risk human papillomaviruses (hrHPVs), Merkel cell polyomavirus (MCPyV), hepatitis B virus (HBV), hepatitis C virus (HCV), Epstein–Barr virus (EBV), Kaposi’s sarcoma-associated herpesvirus (KSHV), and human T-lymphotropic virus 1 (HTLV-1). These viruses impact on several molecular mechanisms in the host cells, often resulting in chronic inflammation, uncontrolled proliferation, and cell death inhibition, and mechanisms, which favor viral life cycle but may indirectly promote tumorigenesis. Recently, the ability of oncogenic viruses to alter autophagy, a catabolic process activated during the innate immune response to infections, is emerging as a key event for the onset of human cancers. Here, we summarize the current understanding of the molecular mechanisms by which human oncogenic viruses regulate autophagy and how this negative regulation impacts on cancer development. Finally, we highlight novel autophagy-related candidates for the treatment of virus-related cancers.

Original languageEnglish
Article number47
Pages (from-to)1-21
Number of pages21
JournalFrontiers in Cell and Developmental Biology
Volume8
DOIs
Publication statusPublished - Feb 28 2020

Keywords

  • autopaghy
  • Epstein–Barr virus (EBV)
  • hepatitis B and C viruses (HBV and HCV)
  • human papillomavirus (HPV)
  • human T-lymphotropic virus 1 (HTLV–1)
  • Kaposi’s sarcoma-associated herpesvirus (KSHV)
  • Merkel cell polyomavirus (MCPyV)
  • oncogenic (or carcinogenic) viruses

ASJC Scopus subject areas

  • Developmental Biology
  • Cell Biology

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