Following the Path of the Virus: The Exploitation of Host DNA Repair Mechanisms by Retroviruses
Abstract
Numerous host cellular cofactors are involved in the life cycle of retroviruses. Importantly, DNA repair machinery of infected cells is activated by retroviruses and retroviral vectors during the process of integration and host cell DNA repair proteins are employed to create a fully integrated provirus. The full delineation of these repair mechanisms that are triggered by retroviruses also has implications outside of the field of retrovirology. It will undoubtedly be of interest to developers of gene therapy and will also further facilitate our understanding of DNA repair and cancer. This review gives a brief summary of the accomplishments in the field of DNA repair and retroviral integration and the opportunities that this area of science provides with regards to the elucidation of repair mechanisms, in the context of retroviral infection.
- Integration: Process of insertion of retroviral DNA into host cell genome.
- Postintegration repair: A process that finalizes the integration of retroviral DNA into host genome.
- Retrovirus: An RNA virus that employs the virus enzyme reverse transcriptase to transcribe the RNA genome into DNA, which then integrates into the host cell’s genome.
- Double strand DNA break: A discontinuity in DNA that involves both DNA strands.
- Nonhomologous end joining: A DNA repair system that involves a large number of proteins and is the major mammalian system for repair of double-strand DNA breaks.
- DNA-PK: DNA-dependent protein kinase. A serine/threonine protein kinase that is activated by double-strand DNA breaks and controls nonhomologous end joining (NHEJ).
- ATM: A DNA-PK-related kinase. ATM stands for ataxia telangiectasia mutated, since its mutation is the underlying cause of ataxia telangiectasia. ATM is involved in repair of double-strand DNA breaks.
- ATR: ATR stands for ATM and Rad3 related. A large serine/threonine kinase that plays a crucial role in DNA repair, including collapsed replication forks and double-strand DNA breaks.
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