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Nat Commun. 2019 Aug 6;10(1):3526. doi: 10.1038/s41467-019-11428-x.
[h=1]Incomplete influenza A virus genomes occur frequently but are readily complemented during localized viral spread.[/h] Jacobs NT[SUP]1[/SUP], Onuoha NO[SUP]1[/SUP], Antia A[SUP]1[/SUP], Steel J[SUP]1,[/SUP][SUP]2[/SUP], Antia R[SUP]3[/SUP], Lowen AC[SUP]4,[/SUP][SUP]5[/SUP].
[h=3]Author information[/h] 1 Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA, USA. 2 Influenza Division, Centers for Disease Control and Prevention, Atlanta, GA, USA. 3 Department of Biology, Emory University, Atlanta, GA, USA. 4 Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA, USA. anice.lowen@emory.edu. 5 Emory-UGA Center of Excellence for Influenza Research and Surveillance, Emory University School of Medicine, Atlanta, GA, USA. anice.lowen@emory.edu.
[h=3]Abstract[/h] Segmentation of viral genomes into multiple RNAs creates the potential for replication of incomplete viral genomes (IVGs). Here we use a single-cell approach to quantify influenza A virus IVGs and examine their fitness implications. We find that each segment of influenza A/Panama/2007/99 (H3N2) virus has a 58% probability of being replicated in a cell infected with a single virion. Theoretical methods predict that IVGs carry high costs in a well-mixed system, as 3.6 virions are required for replication of a full genome. Spatial structure is predicted to mitigate these costs, however, and experimental manipulations of spatial structure indicate that local spread facilitates complementation. A virus entirely dependent on co-infection was used to assess relevance of IVGs in vivo. This virus grows robustly in guinea pigs, but is less infectious and does not transmit. Thus, co-infection allows IVGs to contribute to within-host spread, but complete genomes may be critical for transmission.
PMID: 31387995 PMCID: PMC6684657 DOI: 10.1038/s41467-019-11428-x
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[h=1]Incomplete influenza A virus genomes occur frequently but are readily complemented during localized viral spread.[/h] Jacobs NT[SUP]1[/SUP], Onuoha NO[SUP]1[/SUP], Antia A[SUP]1[/SUP], Steel J[SUP]1,[/SUP][SUP]2[/SUP], Antia R[SUP]3[/SUP], Lowen AC[SUP]4,[/SUP][SUP]5[/SUP].
[h=3]Author information[/h] 1 Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA, USA. 2 Influenza Division, Centers for Disease Control and Prevention, Atlanta, GA, USA. 3 Department of Biology, Emory University, Atlanta, GA, USA. 4 Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA, USA. anice.lowen@emory.edu. 5 Emory-UGA Center of Excellence for Influenza Research and Surveillance, Emory University School of Medicine, Atlanta, GA, USA. anice.lowen@emory.edu.
[h=3]Abstract[/h] Segmentation of viral genomes into multiple RNAs creates the potential for replication of incomplete viral genomes (IVGs). Here we use a single-cell approach to quantify influenza A virus IVGs and examine their fitness implications. We find that each segment of influenza A/Panama/2007/99 (H3N2) virus has a 58% probability of being replicated in a cell infected with a single virion. Theoretical methods predict that IVGs carry high costs in a well-mixed system, as 3.6 virions are required for replication of a full genome. Spatial structure is predicted to mitigate these costs, however, and experimental manipulations of spatial structure indicate that local spread facilitates complementation. A virus entirely dependent on co-infection was used to assess relevance of IVGs in vivo. This virus grows robustly in guinea pigs, but is less infectious and does not transmit. Thus, co-infection allows IVGs to contribute to within-host spread, but complete genomes may be critical for transmission.
PMID: 31387995 PMCID: PMC6684657 DOI: 10.1038/s41467-019-11428-x
Free PMC Article