The Experts below are selected from a list of 6 Experts worldwide ranked by ideXlab platform
Bryan T. Grenfell - One of the best experts on this subject based on the ideXlab platform.
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Phenotypic differences in viral immune escape explained by linking within-Host dynamics to Host-population immunity
Journal of theoretical biology, 2010Co-Authors: Kim M. Pepin, Igor Volkov, Jayanth R. Banavar, Claus O. Wilke, Bryan T. GrenfellAbstract:Viruses that do not cause life-long immunity persist by evolving rapidly in response to prevailing Host immunity. The immune-escape mutants emerge frequently, displacing or co-circulating with native strains even though mutations conferring immune evasion are often detrimental to viral replication. The epidemiological dynamics of immune-escape in acute-infection viruses with high transmissibility have been interpreted mainly through immunity dynamics at the Host population level, despite the fact that immune-escape evolution involves dynamical processes that feedback across the within- and between-Host scales. To address this gap, we use a nested model of within- and between-Host infection dynamics to examine how the interaction of viral replication rate and cross-immunity imprint Host population immunity, which in turn determines viral immune escape. Our explicit consideration of direct and immune-mediated competitive interactions between strains within-Hosts revealed three insights pertaining to risk and control of viral immune-escape: (1) replication rate and immune-stimulation deficiencies (i.e., original antigenic sin) act synergistically to increase immune escape, (2) immune-escape mutants with replication deficiencies relative to their wildtype progenitor are most successful under moderate cross-immunity and frequent re-infections, and (3) the immunity profile along short Host-transmission chains (Local Host-Network structure) is a key determinant of immune escape.
Kim M. Pepin - One of the best experts on this subject based on the ideXlab platform.
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Phenotypic differences in viral immune escape explained by linking within-Host dynamics to Host-population immunity
Journal of theoretical biology, 2010Co-Authors: Kim M. Pepin, Igor Volkov, Jayanth R. Banavar, Claus O. Wilke, Bryan T. GrenfellAbstract:Viruses that do not cause life-long immunity persist by evolving rapidly in response to prevailing Host immunity. The immune-escape mutants emerge frequently, displacing or co-circulating with native strains even though mutations conferring immune evasion are often detrimental to viral replication. The epidemiological dynamics of immune-escape in acute-infection viruses with high transmissibility have been interpreted mainly through immunity dynamics at the Host population level, despite the fact that immune-escape evolution involves dynamical processes that feedback across the within- and between-Host scales. To address this gap, we use a nested model of within- and between-Host infection dynamics to examine how the interaction of viral replication rate and cross-immunity imprint Host population immunity, which in turn determines viral immune escape. Our explicit consideration of direct and immune-mediated competitive interactions between strains within-Hosts revealed three insights pertaining to risk and control of viral immune-escape: (1) replication rate and immune-stimulation deficiencies (i.e., original antigenic sin) act synergistically to increase immune escape, (2) immune-escape mutants with replication deficiencies relative to their wildtype progenitor are most successful under moderate cross-immunity and frequent re-infections, and (3) the immunity profile along short Host-transmission chains (Local Host-Network structure) is a key determinant of immune escape.
Igor Volkov - One of the best experts on this subject based on the ideXlab platform.
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Phenotypic differences in viral immune escape explained by linking within-Host dynamics to Host-population immunity
Journal of theoretical biology, 2010Co-Authors: Kim M. Pepin, Igor Volkov, Jayanth R. Banavar, Claus O. Wilke, Bryan T. GrenfellAbstract:Viruses that do not cause life-long immunity persist by evolving rapidly in response to prevailing Host immunity. The immune-escape mutants emerge frequently, displacing or co-circulating with native strains even though mutations conferring immune evasion are often detrimental to viral replication. The epidemiological dynamics of immune-escape in acute-infection viruses with high transmissibility have been interpreted mainly through immunity dynamics at the Host population level, despite the fact that immune-escape evolution involves dynamical processes that feedback across the within- and between-Host scales. To address this gap, we use a nested model of within- and between-Host infection dynamics to examine how the interaction of viral replication rate and cross-immunity imprint Host population immunity, which in turn determines viral immune escape. Our explicit consideration of direct and immune-mediated competitive interactions between strains within-Hosts revealed three insights pertaining to risk and control of viral immune-escape: (1) replication rate and immune-stimulation deficiencies (i.e., original antigenic sin) act synergistically to increase immune escape, (2) immune-escape mutants with replication deficiencies relative to their wildtype progenitor are most successful under moderate cross-immunity and frequent re-infections, and (3) the immunity profile along short Host-transmission chains (Local Host-Network structure) is a key determinant of immune escape.
Jayanth R. Banavar - One of the best experts on this subject based on the ideXlab platform.
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Phenotypic differences in viral immune escape explained by linking within-Host dynamics to Host-population immunity
Journal of theoretical biology, 2010Co-Authors: Kim M. Pepin, Igor Volkov, Jayanth R. Banavar, Claus O. Wilke, Bryan T. GrenfellAbstract:Viruses that do not cause life-long immunity persist by evolving rapidly in response to prevailing Host immunity. The immune-escape mutants emerge frequently, displacing or co-circulating with native strains even though mutations conferring immune evasion are often detrimental to viral replication. The epidemiological dynamics of immune-escape in acute-infection viruses with high transmissibility have been interpreted mainly through immunity dynamics at the Host population level, despite the fact that immune-escape evolution involves dynamical processes that feedback across the within- and between-Host scales. To address this gap, we use a nested model of within- and between-Host infection dynamics to examine how the interaction of viral replication rate and cross-immunity imprint Host population immunity, which in turn determines viral immune escape. Our explicit consideration of direct and immune-mediated competitive interactions between strains within-Hosts revealed three insights pertaining to risk and control of viral immune-escape: (1) replication rate and immune-stimulation deficiencies (i.e., original antigenic sin) act synergistically to increase immune escape, (2) immune-escape mutants with replication deficiencies relative to their wildtype progenitor are most successful under moderate cross-immunity and frequent re-infections, and (3) the immunity profile along short Host-transmission chains (Local Host-Network structure) is a key determinant of immune escape.
Claus O. Wilke - One of the best experts on this subject based on the ideXlab platform.
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Phenotypic differences in viral immune escape explained by linking within-Host dynamics to Host-population immunity
Journal of theoretical biology, 2010Co-Authors: Kim M. Pepin, Igor Volkov, Jayanth R. Banavar, Claus O. Wilke, Bryan T. GrenfellAbstract:Viruses that do not cause life-long immunity persist by evolving rapidly in response to prevailing Host immunity. The immune-escape mutants emerge frequently, displacing or co-circulating with native strains even though mutations conferring immune evasion are often detrimental to viral replication. The epidemiological dynamics of immune-escape in acute-infection viruses with high transmissibility have been interpreted mainly through immunity dynamics at the Host population level, despite the fact that immune-escape evolution involves dynamical processes that feedback across the within- and between-Host scales. To address this gap, we use a nested model of within- and between-Host infection dynamics to examine how the interaction of viral replication rate and cross-immunity imprint Host population immunity, which in turn determines viral immune escape. Our explicit consideration of direct and immune-mediated competitive interactions between strains within-Hosts revealed three insights pertaining to risk and control of viral immune-escape: (1) replication rate and immune-stimulation deficiencies (i.e., original antigenic sin) act synergistically to increase immune escape, (2) immune-escape mutants with replication deficiencies relative to their wildtype progenitor are most successful under moderate cross-immunity and frequent re-infections, and (3) the immunity profile along short Host-transmission chains (Local Host-Network structure) is a key determinant of immune escape.