Duplication as a source of genetic innovation for «antiviral genes» Volume 20, issue 4, Juillet-Août 2016


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1 Centre international de recherche en infectiologie (CIRI), 46, allée d’Italie, 69364 Lyon, France
2 Inserm, U1111, France
3 École normale supérieure de Lyon, Lyon, France
4 CNRS, UMR5308, France
5 Université de Lyon, Lyon I, UMS3444/US8 BioSciences Gerland, Labex ECOFECT Ecoevolutionary dynamics of infectious diseases, Lyon, France
* Tirés à part

The antiviral proteins, also known as restriction factors, are the primary cellular defense against viral pathogens. These proteins from the innate immune system are in direct interactions with viral proteins. These antagonistic interactions come in two flavors: restriction factors are able to directly target the virus to restrict its replication and/or they may be the target of viral antagonists. Such long-term antagonistic virus-host interactions have set up an evolutionary “arms-race” between the two adversarial entities. This genetic conflict leads to a rapid evolution of viruses and antiviral genes. In particular, amino acids at the virus-host interface change more frequently than expected over time. On the other hand, more drastic host genome modifications have also been selected over time to counteract the rapid evolution of viruses. Reflecting the fact that numerous restriction factors belong to a gene family, it appears that duplication of antiviral genes has occurred frequently during the course of evolution. Here, we will review how duplication of antiviral genes has been selected in the host and how the divergence and plasticity of the duplicated genes may have been advantageous in the virus-host genetic conflict. We will also briefly expose the limits to such innate immune gene expansion.