tetano
Editor, Senior Moderator
J Gen Virol. 2014 Aug 18. pii: vir.0.067694-0. doi: 10.1099/vir.0.067694-0. [Epub ahead of print]
Two amino acid substitutions in the hemagglutinin of the 2009 pandemic H1N1 virus decrease direct-contact transmission in guinea pigs.
He L1, Jiang K1, Wu Q1, Duan Z1, Xu H1, Liu J1, Cui Z1, Gu M1, Wang X1, Liu X1, Liu X2.
Author information
Abstract
The 2009 pandemic H1N1 influenza A virus spread across the globe and caused the first influenza pandemic of the 21st century. Many of the molecular factors that contributed to the airborne transmission of this pandemic virus have been determined; however, the direct-contact transmission of this virus remains poorly understood. In this study, we report that a combination of two mutations (N159D and Q226R) in the hemagglutinin (HA) protein of the representative 2009 H1N1 influenza virus A/California/04/2009 (CA04) caused a switch in receptor binding preference from the α2,6-sialoglycan to the α2,3-sialoglycan receptor and decreased the binding intensities for both glycans. In conjunction with a significantly decreased replication efficiency in the nasal epithelium, this limited human receptor-binding affinity resulted in inefficient direct-contact transmission of CA04 between guinea pigs. Our findings highlight the role of the HA gene in the transmission of the influenza virus.
Copyright ? 2014, the Society for General Microbiology.
KEYWORDS:
2009 pandemic H1N1 virus; direct-contact transmission; hemagglutinin; mutations
PMID:
25135885
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/25135885
Two amino acid substitutions in the hemagglutinin of the 2009 pandemic H1N1 virus decrease direct-contact transmission in guinea pigs.
He L1, Jiang K1, Wu Q1, Duan Z1, Xu H1, Liu J1, Cui Z1, Gu M1, Wang X1, Liu X1, Liu X2.
Author information
Abstract
The 2009 pandemic H1N1 influenza A virus spread across the globe and caused the first influenza pandemic of the 21st century. Many of the molecular factors that contributed to the airborne transmission of this pandemic virus have been determined; however, the direct-contact transmission of this virus remains poorly understood. In this study, we report that a combination of two mutations (N159D and Q226R) in the hemagglutinin (HA) protein of the representative 2009 H1N1 influenza virus A/California/04/2009 (CA04) caused a switch in receptor binding preference from the α2,6-sialoglycan to the α2,3-sialoglycan receptor and decreased the binding intensities for both glycans. In conjunction with a significantly decreased replication efficiency in the nasal epithelium, this limited human receptor-binding affinity resulted in inefficient direct-contact transmission of CA04 between guinea pigs. Our findings highlight the role of the HA gene in the transmission of the influenza virus.
Copyright ? 2014, the Society for General Microbiology.
KEYWORDS:
2009 pandemic H1N1 virus; direct-contact transmission; hemagglutinin; mutations
PMID:
25135885
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/25135885