tetano
Editor, Senior Moderator
Proc Natl Acad Sci U S A. 2014 Nov 10. pii: 201415396. [Epub ahead of print]
Influenza A virus nucleoprotein selectively decreases neuraminidase gene-segment packaging while enhancing viral fitness and transmissibility.
Brooke CB1, Ince WL1, Wei J1, Bennink JR1, Yewdell JW2.
Author information
Abstract
The influenza A virus (IAV) genome is divided into eight distinct RNA segments believed to be copackaged into virions with nearly perfect efficiency. Here, we describe a mutation in IAV nucleoprotein (NP) that enhances replication and transmission in guinea pigs while selectively reducing neuraminidase (NA) gene segment packaging into virions. We show that incomplete IAV particles lacking gene segments contribute to the propagation of the viral population through multiplicity reactivation under conditions of widespread coinfection, which we demonstrate commonly occurs in the upper respiratory tract of guinea pigs. NP also dramatically altered the functional balance of the viral glycoproteins on particles by selectively decreasing NA expression. Our findings reveal novel functions for NP in selective control of IAV gene packaging and balancing glycoprotein expression and suggest a role for incomplete gene packaging during host adaptation and transmission.
KEYWORDS:
genome packaging; genome segmentation; host adaptation; influenza virus; nucleoprotein
PMID:
25385602
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/25385602
Influenza A virus nucleoprotein selectively decreases neuraminidase gene-segment packaging while enhancing viral fitness and transmissibility.
Brooke CB1, Ince WL1, Wei J1, Bennink JR1, Yewdell JW2.
Author information
Abstract
The influenza A virus (IAV) genome is divided into eight distinct RNA segments believed to be copackaged into virions with nearly perfect efficiency. Here, we describe a mutation in IAV nucleoprotein (NP) that enhances replication and transmission in guinea pigs while selectively reducing neuraminidase (NA) gene segment packaging into virions. We show that incomplete IAV particles lacking gene segments contribute to the propagation of the viral population through multiplicity reactivation under conditions of widespread coinfection, which we demonstrate commonly occurs in the upper respiratory tract of guinea pigs. NP also dramatically altered the functional balance of the viral glycoproteins on particles by selectively decreasing NA expression. Our findings reveal novel functions for NP in selective control of IAV gene packaging and balancing glycoprotein expression and suggest a role for incomplete gene packaging during host adaptation and transmission.
KEYWORDS:
genome packaging; genome segmentation; host adaptation; influenza virus; nucleoprotein
PMID:
25385602
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/25385602