tetano
Editor, Senior Moderator
Genetics. 2018 Sep 4. pii: genetics.301510.2018. doi: 10.1534/genetics.118.301510. [Epub ahead of print]
[h=1]Effects of Transmission Bottlenecks on the Diversity of Influenza A Virus.[/h] Sigal D[SUP]1[/SUP], Reid JNS[SUP]1[/SUP], Wahl LM[SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] We investigate the fate of de novo mutations that occur during the in-host replication of a pathogenic virus, predicting the probability that such mutations are passed on during disease transmission to a new host. Using influenza A virus as a model organism, we develop a life-history model of the within-host dynamics of the infection, deriving a multitype branching process with a coupled deterministic model to capture the population of available target cells. We quantify the fate of neutral mutations and mutations affecting five life-history traits: clearance, attachment, budding, cell death, and eclipse phase timing. Despite the severity of disease transmission bottlenecks, our results suggest that in a single transmission event, several mutations that appeared de novo in the donor are likely to be transmitted to the recipient. Even in the absence of a selective advantage for these mutations, the sustained growth phase inherent in each disease transmission cycle generates genetic diversity that is not eliminated during the transmission bottleneck.
[h=4]KEYWORDS:[/h] adaptation; disease transmission; influenza; life history; mutation
PMID: 30181193 DOI: 10.1534/genetics.118.301510
Free full text
[h=1]Effects of Transmission Bottlenecks on the Diversity of Influenza A Virus.[/h] Sigal D[SUP]1[/SUP], Reid JNS[SUP]1[/SUP], Wahl LM[SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] We investigate the fate of de novo mutations that occur during the in-host replication of a pathogenic virus, predicting the probability that such mutations are passed on during disease transmission to a new host. Using influenza A virus as a model organism, we develop a life-history model of the within-host dynamics of the infection, deriving a multitype branching process with a coupled deterministic model to capture the population of available target cells. We quantify the fate of neutral mutations and mutations affecting five life-history traits: clearance, attachment, budding, cell death, and eclipse phase timing. Despite the severity of disease transmission bottlenecks, our results suggest that in a single transmission event, several mutations that appeared de novo in the donor are likely to be transmitted to the recipient. Even in the absence of a selective advantage for these mutations, the sustained growth phase inherent in each disease transmission cycle generates genetic diversity that is not eliminated during the transmission bottleneck.
[h=4]KEYWORDS:[/h] adaptation; disease transmission; influenza; life history; mutation
PMID: 30181193 DOI: 10.1534/genetics.118.301510
Free full text