-
- Santiago F Elena
- Instituto de Biología Molecular y Celular de Plantas (CSIC‐UPV), Avenida de los Naranjos s/n 46022 València Spain
-
- Purificación Carrasco
- Instituto de Biología Molecular y Celular de Plantas (CSIC‐UPV), Avenida de los Naranjos s/n 46022 València Spain
-
- José‐Antonio Daròs
- Instituto de Biología Molecular y Celular de Plantas (CSIC‐UPV), Avenida de los Naranjos s/n 46022 València Spain
-
- Rafael Sanjuán
- Instituto de Biología Molecular y Celular de Plantas (CSIC‐UPV), Avenida de los Naranjos s/n 46022 València Spain
説明
<jats:p>Two key features of RNA viruses are their compacted genomes and their high mutation rate. Accordingly, deleterious mutations are common and have an enormous impact on viral fitness. In their multicellular hosts, robustness can be achieved by genomic redundancy, including gene duplication, diploidy, alternative metabolic pathways and biochemical buffering mechanisms. However, here we review evidence suggesting that during RNA virus evolution, alternative robustness mechanisms may have been selected. After briefly describing how genetic robustness can be quantified, we discuss mechanisms of intrinsic robustness arising as consequences of RNA‐genome architecture, replication peculiarities and quasi‐species population dynamics. These intrinsic robustness mechanisms operate efficiently at the population level, despite the mutational sensitivity shown by individual genomes. Finally, we discuss the possibility that viruses might exploit cellular buffering mechanisms for their own benefit, producing a sort of extrinsic robustness.</jats:p>
収録刊行物
-
- EMBO reports
-
EMBO reports 7 (2), 168-173, 2006-02
Springer Science and Business Media LLC
