2026-04-17T05:22:08Zhttps://recercat.cat/oai/request

oai:recercat.cat:10230/255462025-12-18T01:10:04Zcom_2072_6col_2072_452952

00925njm 22002777a 4500 dc Elena, Santiago F. author Solé Vicente, Ricard, 1962- author Sardanyés i Cayuela, Josep author 2016-01-11T13:23:27Z 2016-01-11T13:23:27Z 2010 Owed to their reduced size and low number of proteins encoded, RNA viruses and other subviral pathogens are often considered as being genetically too simple. However, this structural simplicity also creates the necessity for viral RNA sequences to encode for more than one protein and for proteins to carry out multiple functions, all together resulting in complex patterns of genetic interactions. In this work we will first review the experimental studies revealing that the architecture of viral genomes is dominated by antagonistic interactions among loci. Second, we will also review mathematical models and provide a description of computational tools for the study of RNA virus dynamics and evolution. As an application of these tools, we will finish this review article by analyzing a stochastic bit-string model of in silico virus replication. This model analyzes the interplay between epistasis and the mode of replication on determining the population load of deleterious mutations. The model suggests that, for a given mutation rate, the deleterious mutational load is always larger when epistasis is predominantly antagonistic than when synergism is the rule. However, the magnitude of this effect is larger if replication occurs geometrically than if it proceeds linearly. Evolució (Biologia) RNA Simple genomes, complex interactions: epistasis in RNA virus