tetano
Editor, Senior Moderator
Virology. 2012 Jul 16. [Epub ahead of print]
Both influenza hemagglutinin and polymerase acidic genes are important for delayed pandemic 2009 H1N1 virus clearance in the ferret model.
Ducatez MF, Ilyushina NA, Fabrizio TP, Rehg JE, Bovin NV, Webster RG, Webby RJ.
Source
Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN 38105-3678, USA.
Abstract
We previously showed that a pandemic virus, A/Tennessee/560/09(H1N1), had the potential to adapt to human bronchial epithelial cells by the acquisition of hemagglutinin (HA) K154Q and polymerase acidic (PA) protein L295P mutations that conferred a more virulent phenotype. To better elucidate the role of each mutations, we generated recombinant viruses carrying single mutations or both mutations concurrently. The replication of all mutant viruses was significantly higher than that of the wild-type A/Tennessee/560/09 virus in human cells. The HA K154Q mutation reduced the receptor binding affinity of A/Tennessee/560/09 virus to 6-Su-6'SLN and biantennary 6'SLN receptors. In ferrets, H1N1 virus with HA K154Q and PA L295P mutations exhibited significantly higher titers in the upper respiratory tract compared to all other viruses 6 days post-infection. Our results suggest that both single mutations HA K154Q and PA L295P are necessary for delayed virus clearance of A/Tennessee/560/09(H1N1) influenza virus in a ferret animal model.
Copyright ? 2012 Elsevier Inc. All rights reserved.
PMID:
22809692
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22809692
Both influenza hemagglutinin and polymerase acidic genes are important for delayed pandemic 2009 H1N1 virus clearance in the ferret model.
Ducatez MF, Ilyushina NA, Fabrizio TP, Rehg JE, Bovin NV, Webster RG, Webby RJ.
Source
Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN 38105-3678, USA.
Abstract
We previously showed that a pandemic virus, A/Tennessee/560/09(H1N1), had the potential to adapt to human bronchial epithelial cells by the acquisition of hemagglutinin (HA) K154Q and polymerase acidic (PA) protein L295P mutations that conferred a more virulent phenotype. To better elucidate the role of each mutations, we generated recombinant viruses carrying single mutations or both mutations concurrently. The replication of all mutant viruses was significantly higher than that of the wild-type A/Tennessee/560/09 virus in human cells. The HA K154Q mutation reduced the receptor binding affinity of A/Tennessee/560/09 virus to 6-Su-6'SLN and biantennary 6'SLN receptors. In ferrets, H1N1 virus with HA K154Q and PA L295P mutations exhibited significantly higher titers in the upper respiratory tract compared to all other viruses 6 days post-infection. Our results suggest that both single mutations HA K154Q and PA L295P are necessary for delayed virus clearance of A/Tennessee/560/09(H1N1) influenza virus in a ferret animal model.
Copyright ? 2012 Elsevier Inc. All rights reserved.
PMID:
22809692
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22809692