tetano
Editor, Senior Moderator
Influenza Other Respi Viruses. 2012 Feb 21. doi: 10.1111/j.1750-2659.2012.00333.x. [Epub ahead of print]
Infectivity phenotypes of H3N2 influenza A viruses in primary swine respiratory epithelial cells are controlled by sialic acid binding.
Bateman AC, Busch MG, Karasin AI, Olsen CW.
Source
Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, WI, USA.
Abstract
Please cite this paper as: Bateman et al. (2012) Infectivity phenotypes of H3N2 influenza A viruses in primary swine respiratory epithelial cells are controlled by sialic acid binding. Influenza and Other Respiratory Viruses DOI: 10.1111/j.1750-2659.2012.00333.x. Background In the late 1990s, triple reassortant H3N2 influenza A viruses emerged and spread widely in the US swine population. We have shown previously that an isolate representative of this virus-lineage, A/Swine/Minnesota/593/99 (Sw/MN), exhibits phenotypic differences compared to a wholly human-lineage H3N2 virus isolated during the same time period, A/Swine/Ontario/00130/97 (Sw/ONT). Specifically, Sw/MN was more infectious for pigs and infected a significantly higher proportion of cultured primary swine respiratory epithelial cells (SRECs). In addition, reverse genetics-generated Sw/MN ? Sw/ONT reassortant and point mutant viruses demonstrated that the infectivity phenotypes in SRECs were strongly dependent on three amino acids within the hemagglutinin (HA) gene. Objectives To determine the mechanism by which Sw/MN attains higher infectivity than Sw/ONT in SRECs. Methods A/Swine/Minnesota/593/99, Sw/ONT, and mutant (reverse genetics-generated HA reassortant and point mutant) viruses were compared at various HA-mediated stages of infection: initial sialic acid binding, virus entry, and the pH of virus-endosome fusion. Results/Conclusions Sialic acid binding was the sole stage where virus differences directly paralleled infectivity phenotypes in SRECs, indicating that binding is the primary mechanism responsible for differences in the infectivity levels of Sw/MN and Sw/ONT.
? 2012 Blackwell Publishing Ltd.
PMID:
22353399
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22353399
Infectivity phenotypes of H3N2 influenza A viruses in primary swine respiratory epithelial cells are controlled by sialic acid binding.
Bateman AC, Busch MG, Karasin AI, Olsen CW.
Source
Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, WI, USA.
Abstract
Please cite this paper as: Bateman et al. (2012) Infectivity phenotypes of H3N2 influenza A viruses in primary swine respiratory epithelial cells are controlled by sialic acid binding. Influenza and Other Respiratory Viruses DOI: 10.1111/j.1750-2659.2012.00333.x. Background In the late 1990s, triple reassortant H3N2 influenza A viruses emerged and spread widely in the US swine population. We have shown previously that an isolate representative of this virus-lineage, A/Swine/Minnesota/593/99 (Sw/MN), exhibits phenotypic differences compared to a wholly human-lineage H3N2 virus isolated during the same time period, A/Swine/Ontario/00130/97 (Sw/ONT). Specifically, Sw/MN was more infectious for pigs and infected a significantly higher proportion of cultured primary swine respiratory epithelial cells (SRECs). In addition, reverse genetics-generated Sw/MN ? Sw/ONT reassortant and point mutant viruses demonstrated that the infectivity phenotypes in SRECs were strongly dependent on three amino acids within the hemagglutinin (HA) gene. Objectives To determine the mechanism by which Sw/MN attains higher infectivity than Sw/ONT in SRECs. Methods A/Swine/Minnesota/593/99, Sw/ONT, and mutant (reverse genetics-generated HA reassortant and point mutant) viruses were compared at various HA-mediated stages of infection: initial sialic acid binding, virus entry, and the pH of virus-endosome fusion. Results/Conclusions Sialic acid binding was the sole stage where virus differences directly paralleled infectivity phenotypes in SRECs, indicating that binding is the primary mechanism responsible for differences in the infectivity levels of Sw/MN and Sw/ONT.
? 2012 Blackwell Publishing Ltd.
PMID:
22353399
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22353399