Human papillomaviruses target the dna damage repair and innate immune response pathways to allow for persistent infection

Elona Gusho, Laimonis Laimins*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

4 Scopus citations

Abstract

Persistent infection with high-risk human papillomaviruses (HPVs) is the major risk factor associated with development of anogenital and oropharyngeal cancers. Initial infection by HPVs occurs into basal epithelial cells where viral genomes are established as nuclear episomes and per-sist until cleared by the immune response. Productive replication or amplification occurs upon differentiation and is dependent upon activation of the ataxia-telangiectasia mutated (ATM), ataxia telangiectasia and RAD3-related (ATR) DNA damage repair (DDR) pathways. In addition to activat-ing DDR pathways, HPVs must escape innate immune surveillance mechanisms by antagonizing sensors, adaptors, interferons and antiviral gene expression. Both DDR and innate immune pathways are key host mechanisms that crosstalk with each other to maintain homeostasis of cells persistently infected with HPVs. Interestingly, it is still not fully understood why some HPV infections get cleared while others do not. Targeting of these two processes with antiviral therapies may provide opportunities for treatment of cancers caused by high-risk HPVs.

Original languageEnglish (US)
Article number1390
JournalViruses
Volume13
Issue number7
DOIs
StatePublished - Jul 2021

Keywords

  • DAMPs
  • DNA damage
  • Epithelial differentiation
  • HPVs
  • Innate immunity

ASJC Scopus subject areas

  • Infectious Diseases
  • Virology

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