4.6 Review

APOBEC3 Interference during Replication of Viral Genomes

期刊

VIRUSES-BASEL
卷 7, 期 6, 页码 2999-3018

出版社

MDPI
DOI: 10.3390/v7062757

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资金

  1. Fonds National de la Recherche Scientifique (FNRS)
  2. Televie
  3. Interuniversity Attraction Poles (IAP) Program Virus-host interplay at the early phases of infection BELVIR
  4. Belgian Science Policy Office
  5. Belgian Foundation against Cancer (FBC)
  6. European Union [INCA LSHC-CT-2005-018704]
  7. Neoangio excellence program
  8. Direction generale des Technologies, de la Recherche et de L'Energie/DG06 of the Walloon government
  9. Action de Recherche Concertee Glyvir (ARC) of the Communaute francaise de Belgique
  10. Centre anticancereux pres ULg (CAC)
  11. Gembloux Agrobiotech (GxABT)
  12. ULg Fonds Speciaux pour la Recherche
  13. Plan Cancer of the Service Public Federal

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Co-evolution of viruses and their hosts has reached a fragile and dynamic equilibrium that allows viral persistence, replication and transmission. In response, infected hosts have developed strategies of defense that counteract the deleterious effects of viral infections. In particular, single-strand DNA editing by Apolipoprotein B Editing Catalytic subunits proteins 3 (APOBEC3s) is a well-conserved mechanism of mammalian innate immunity that mutates and inactivates viral genomes. In this review, we describe the mechanisms of APOBEC3 editing during viral replication, the viral strategies that prevent APOBEC3 activity and the consequences of APOBEC3 modulation on viral fitness and host genome integrity. Understanding the mechanisms involved reveals new prospects for therapeutic intervention.

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