Influenza A Virus Transmission Bottlenecks Are Defined by Infection Route and Recipient Host
Despite its global relevance, our understanding of how influenza A virus transmission impacts the overall population dynamics of this RNA virus remains incomplete. To define this dynamic, we inserted neutral barcodes into the influenza A virus genome to generate a population of viruses that can be i...
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Published in | Cell host & microbe Vol. 16; no. 5; pp. 691 - 700 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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United States
Elsevier Inc
12.11.2014
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Subjects | |
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Abstract | Despite its global relevance, our understanding of how influenza A virus transmission impacts the overall population dynamics of this RNA virus remains incomplete. To define this dynamic, we inserted neutral barcodes into the influenza A virus genome to generate a population of viruses that can be individually tracked during transmission events. We find that physiological bottlenecks differ dramatically based on the infection route and level of adaptation required for efficient replication. Strong genetic pressures are responsible for bottlenecks during adaptation across different host species, whereas transmission between susceptible hosts results in bottlenecks that are not genetically driven and occur at the level of the recipient. Additionally, the infection route significantly influences the bottleneck stringency, with aerosol transmission imposing greater selection than direct contact. These transmission constraints have implications in understanding the global migration of virus populations and provide a clearer perspective on the emergence of pandemic strains.
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•Influenza A virus transmission involves sequence-dependent and -independent bottlenecks•The transmission route affects bottleneck stringency and initial virus population diversity•Virus population selection during transmission occurs at the level of recipient
The biology of virus transmission impacts geographical spread and genetic diversity. By examining influenza A virus populations during different transmission events, Varble et al. find that bottlenecks differ based on the level of adaptation required for virus replication and the infection route. |
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AbstractList | Despite its global relevance, our understanding of how influenza A virus transmission impacts the overall population dynamics of this RNA virus remains incomplete. To define this dynamic, we inserted neutral barcodes into the influenza A virus genome to generate a population of viruses that can be individually tracked during transmission events. We find that physiological bottlenecks differ dramatically based on the infection route and level of adaptation required for efficient replication. Strong genetic pressures are responsible for bottlenecks during adaptation across different host species, whereas transmission between susceptible hosts results in bottlenecks that are not genetically driven and occur at the level of the recipient. Additionally, the infection route significantly influences the bottleneck stringency, with aerosol transmission imposing greater selection than direct contact. These transmission constraints have implications in understanding the global migration of virus populations and provide a clearer perspective on the emergence of pandemic strains.Despite its global relevance, our understanding of how influenza A virus transmission impacts the overall population dynamics of this RNA virus remains incomplete. To define this dynamic, we inserted neutral barcodes into the influenza A virus genome to generate a population of viruses that can be individually tracked during transmission events. We find that physiological bottlenecks differ dramatically based on the infection route and level of adaptation required for efficient replication. Strong genetic pressures are responsible for bottlenecks during adaptation across different host species, whereas transmission between susceptible hosts results in bottlenecks that are not genetically driven and occur at the level of the recipient. Additionally, the infection route significantly influences the bottleneck stringency, with aerosol transmission imposing greater selection than direct contact. These transmission constraints have implications in understanding the global migration of virus populations and provide a clearer perspective on the emergence of pandemic strains. Despite its global relevance, our understanding of how influenza A virus transmission impacts the overall population dynamics of this RNA virus remains incomplete. To define this dynamic, we inserted neutral barcodes into the influenza A virus genome to generate a population of viruses that can be individually tracked during transmission events. We find that physiological bottlenecks differ dramatically based on the infection route and level of adaptation required for efficient replication. Strong genetic pressures are responsible for bottlenecks during adaptation across different host species, whereas transmission between susceptible hosts results in bottlenecks that are not genetically driven and occur at the level of the recipient. Additionally, the infection route significantly influences the bottleneck stringency, with aerosol transmission imposing greater selection than direct contact. These transmission constraints have implications in understanding the global migration of virus populations and provide a clearer perspective on the emergence of pandemic strains. [Display omitted] •Influenza A virus transmission involves sequence-dependent and -independent bottlenecks•The transmission route affects bottleneck stringency and initial virus population diversity•Virus population selection during transmission occurs at the level of recipient The biology of virus transmission impacts geographical spread and genetic diversity. By examining influenza A virus populations during different transmission events, Varble et al. find that bottlenecks differ based on the level of adaptation required for virus replication and the infection route. Despite its global relevance, our understanding of how influenza A virus transmission impacts the overall population dynamics of this RNA virus remains incomplete. To define this dynamic, we inserted neutral barcodes into the influenza A virus genome to generate a population of viruses that can be individually tracked during transmission events. We find that physiological bottlenecks differ dramatically based on the infection route and level of adaptation required for efficient replication. Strong genetic pressures are responsible for bottlenecks during adaptation across different host species, whereas transmission between susceptible hosts results in bottlenecks that are not genetically driven and occur at the level of the recipient. Additionally, the infection route significantly influences the bottleneck stringency, with aerosol transmission imposing greater selection than direct contact. These transmission constraints have implications in understanding the global migration of virus populations and provide a clearer perspective into the emergence of pandemic strains. Despite its global relevance, our understanding of how influenza A virus transmission impacts the overall population dynamics of this RNA virus remains incomplete. To define this dynamic, we inserted neutral barcodes into the influenza A virus genome to generate a population of viruses that can be individually tracked during transmission events. We find that physiological bottlenecks differ dramatically based on the infection route and level of adaptation required for efficient replication. Strong genetic pressures are responsible for bottlenecks during adaptation across different host species, whereas transmission between susceptible hosts results in bottlenecks that are not genetically driven and occur at the level of the recipient. Additionally, the infection route significantly influences the bottleneck stringency, with aerosol transmission imposing greater selection than direct contact. These transmission constraints have implications in understanding the global migration of virus populations and provide a clearer perspective on the emergence of pandemic strains. |
Author | Albrecht, Randy A. García-Sastre, Adolfo Crumiller, Marshall Backes, Simone Sachs, David tenOever, Benjamin R. Bouvier, Nicole M. Varble, Andrew |
AuthorAffiliation | 5 Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, 10029 USA 1 Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, New York, 10029 USA 3 The Laboratory of Biophysics, The Rockefeller University, New York, NY, 10065 USA 2 Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, New York, 10029 USA 4 Department of Medicine, Division of Infectious Diseases, Icahn School of Medicine at Mount Sinai, New York, New York, 10029 USA |
AuthorAffiliation_xml | – name: 2 Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, New York, 10029 USA – name: 3 The Laboratory of Biophysics, The Rockefeller University, New York, NY, 10065 USA – name: 5 Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, 10029 USA – name: 4 Department of Medicine, Division of Infectious Diseases, Icahn School of Medicine at Mount Sinai, New York, New York, 10029 USA – name: 1 Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, New York, 10029 USA |
Author_xml | – sequence: 1 givenname: Andrew surname: Varble fullname: Varble, Andrew organization: Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA – sequence: 2 givenname: Randy A. surname: Albrecht fullname: Albrecht, Randy A. organization: Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA – sequence: 3 givenname: Simone surname: Backes fullname: Backes, Simone organization: Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA – sequence: 4 givenname: Marshall surname: Crumiller fullname: Crumiller, Marshall organization: The Laboratory of Biophysics, The Rockefeller University, New York, NY 10065, USA – sequence: 5 givenname: Nicole M. surname: Bouvier fullname: Bouvier, Nicole M. organization: Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA – sequence: 6 givenname: David surname: Sachs fullname: Sachs, David organization: Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA – sequence: 7 givenname: Adolfo surname: García-Sastre fullname: García-Sastre, Adolfo organization: Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA – sequence: 8 givenname: Benjamin R. surname: tenOever fullname: tenOever, Benjamin R. email: benjamin.tenoever@mssm.edu organization: Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25456074$$D View this record in MEDLINE/PubMed |
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SubjectTerms | Animals Cell Line, Tumor Disease Transmission, Infectious - veterinary DNA Barcoding, Taxonomic Dogs Ferrets Genome, Viral Guinea Pigs High-Throughput Nucleotide Sequencing Host-Pathogen Interactions Humans Influenza A virus - genetics Influenza A virus - pathogenicity Influenza, Human - transmission Madin Darby Canine Kidney Cells Male Orthomyxoviridae Infections - transmission |
Title | Influenza A Virus Transmission Bottlenecks Are Defined by Infection Route and Recipient Host |
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