baldassarri baronchelli barrat caglioti castellano cattuto complexity dattoli evolutionary_dynamics granular_media granular_media herrmann information_theory innovation_dynamics kreyon language_dynamics loreto mari mukherjee petri pietronero puglisi quantum_optics self_organization servedio statistical_physics techno_social_systems tria zapperi zippers
2013 |
Taggi, Lorenzo; Colaiori, Francesca; Loreto, Vittorio; Tria, Francesca Dynamical correlations in the escape strategy of Influenza A virus Journal Article EUROPHYSICS LETTERS, 101 , 2013. Abstract | BibTeX | Tag: biology, colaiori, evolutionary_dynamics, loreto, taggi, tria @article{b, title = {Dynamical correlations in the escape strategy of Influenza A virus}, author = {Lorenzo Taggi and Francesca Colaiori and Vittorio Loreto and Francesca Tria}, year = {2013}, date = {2013-01-01}, journal = {EUROPHYSICS LETTERS}, volume = {101}, abstract = {The evolutionary dynamics of human Influenza A virus presents a challenging theoretical problem. An extremely high mutation rate allows the virus to escape, at each epidemic season, the host immune protection elicited by previous infections. At the same time, at each given epidemic season a single quasi-species, that is a set of closely related strains, is observed. A non-trivial relation between the genetic (i.e., at the sequence level) and the antigenic (i.e., related to the host immune response) distances can shed light into this puzzle. In this paper we introduce a model in which, in accordance with experimental observations, a simple interaction rule based on spatial correlations among point mutations dynamically defines an immunity space in the space of sequences. We investigate the static and dynamic structure of this space and we discuss how it affects the dynamics of the virus-host interaction. Interestingly we observe a staggered time structure in the virus evolution as in the real Influenza evolutionary dynamics. © Copyright EPLA, 2013.}, keywords = {biology, colaiori, evolutionary_dynamics, loreto, taggi, tria}, pubstate = {published}, tppubtype = {article} } The evolutionary dynamics of human Influenza A virus presents a challenging theoretical problem. An extremely high mutation rate allows the virus to escape, at each epidemic season, the host immune protection elicited by previous infections. At the same time, at each given epidemic season a single quasi-species, that is a set of closely related strains, is observed. A non-trivial relation between the genetic (i.e., at the sequence level) and the antigenic (i.e., related to the host immune response) distances can shed light into this puzzle. In this paper we introduce a model in which, in accordance with experimental observations, a simple interaction rule based on spatial correlations among point mutations dynamically defines an immunity space in the space of sequences. We investigate the static and dynamic structure of this space and we discuss how it affects the dynamics of the virus-host interaction. Interestingly we observe a staggered time structure in the virus evolution as in the real Influenza evolutionary dynamics. © Copyright EPLA, 2013. |
Tria, Francesca; Pompei, Simone; Loreto, Vittorio Dynamically correlated mutations drive human Influenza A evolution Journal Article SCIENTIFIC REPORTS, 3 , 2013. Abstract | Links | BibTeX | Tag: biology, evolutionary_dynamics, loreto, pompei, tria @article{b, title = {Dynamically correlated mutations drive human Influenza A evolution}, author = {Francesca Tria and Simone Pompei and Vittorio Loreto}, url = {http://www.nature.com/srep/2013/130919/srep02705/full/srep02705.html}, year = {2013}, date = {2013-01-01}, journal = {SCIENTIFIC REPORTS}, volume = {3}, publisher = {NATURE PUBLISHING GROUP}, abstract = {Human Influenza A virus undergoes recurrent changes in the hemagglutinin (HA) surface protein, primarily involved in the human antibody recognition. Relevant antigenic changes, enabling the virus to evade host immune response, have been recognized to occur in parallel to multiple mutations at antigenic sites in HA. Yet, the role of correlated mutations (epistasis) in driving the molecular evolution of the virus still represents a challenging puzzle. Further, though circulation at a global geographic level is key for the survival of Influenza A, its role in shaping the viral phylodynamics remains largely unexplored. Here we show, through a sequence based epidemiological model, that epistatic effects between amino acids substitutions, coupled with a reservoir that mimics worldwide circulating viruses, are key determinants that drive human Influenza A evolution. Our approach explains all the up-to-date observations characterizing the evolution of H3N2 subtype, including phylogenetic properties, nucleotide fixation patterns, and composition of antigenic clusters.}, keywords = {biology, evolutionary_dynamics, loreto, pompei, tria}, pubstate = {published}, tppubtype = {article} } Human Influenza A virus undergoes recurrent changes in the hemagglutinin (HA) surface protein, primarily involved in the human antibody recognition. Relevant antigenic changes, enabling the virus to evade host immune response, have been recognized to occur in parallel to multiple mutations at antigenic sites in HA. Yet, the role of correlated mutations (epistasis) in driving the molecular evolution of the virus still represents a challenging puzzle. Further, though circulation at a global geographic level is key for the survival of Influenza A, its role in shaping the viral phylodynamics remains largely unexplored. Here we show, through a sequence based epidemiological model, that epistatic effects between amino acids substitutions, coupled with a reservoir that mimics worldwide circulating viruses, are key determinants that drive human Influenza A evolution. Our approach explains all the up-to-date observations characterizing the evolution of H3N2 subtype, including phylogenetic properties, nucleotide fixation patterns, and composition of antigenic clusters. |
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