Dataset Information

Characterization and Evolutionary Analysis of a Novel H3N2 Influenza A Virus Glycosylation Motif in Southern China.

ABSTRACT: An influenza A (H3N2) virus epidemic occurred in China in 2017 and the causative strain failed to bind red blood cells (RBCs), which may affect receptor binding and antibody recognition. The objective of this study was to analyze the genetic characteristics and glycosylation changes of this novel H3N2 strain. We directly sequenced the hemagglutinin (HA) genes of H3N2 clinical specimens collected from patients with acute respiratory tract infection during 2017 in Guangdong, China. We aligned these sequences with those of A/Hong Kong/1/1968 (H3N2) and A/Brisbane/10/2007 (H3N2). Glycosylation changes were analyzed by C18 Chip-Q-TOF-MS. A/China/LZP/2017 (H3N2) was negative by HA assay, but was positive by quantitative real-time Polymerase Chain Reaction (qPCR) and direct immunofluorescence assay (DFA). We found that the HA1 residue 160T of A/China/LZP/2017 (H3N2) could block virus binding to receptors on RBCs. Furthermore, the ASN (N)-X-Thr (T) motif at HA1 residues 158-160, encoding a glycosylation site as shown by C18 Chip-Q-TOF-MS, predominated worldwide and played a critical role in RBC receptor binding. Ten glycoforms at HA1 residue 158 were identified [4_3_1_0, 5_6_0_1, 3_3_0_1, 4_4_3_0, 6_7_0_0 (SO3), 3_6_2_0, 4_3_1_2 (SO3), 7_5_2_0 (SO3), 3_6_2_1 (SO3), and 3_7_0_2]. Glycosylation changes at HA1 residues 158-160 of a circulating influenza A (H3N2) virus in Guangdong, China, in 2017 blocked binding to RBC receptors. Changes to these HA1 residues may have reduced protective antibody responses as well. Understanding these critical epitopes is important for selecting vaccine strains.

SUBMITTER: Zeng Z

PROVIDER: S-EPMC7309185 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Characterization and Evolutionary Analysis of a Novel H3N2 Influenza A Virus Glycosylation Motif in Southern China.

Zeng Zhiqi Z Yau Lee-Fong LF Lin Zengxian Z Xia Xuanzi X Yang Zifeng Z Wang Jing-Rong JR Song Wenjun W Wang Xinhua X

Frontiers in microbiology 20200616

An influenza A (H3N2) virus epidemic occurred in China in 2017 and the causative strain failed to bind red blood cells (RBCs), which may affect receptor binding and antibody recognition. The objective of this study was to analyze the genetic characteristics and glycosylation changes of this novel H3N2 strain. We directly sequenced the hemagglutinin (HA) genes of H3N2 clinical specimens collected from patients with acute respiratory tract infection during 2017 in Guangdong, China. We aligned thes ...[more]

PMID: 32612596

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Project description:UnlabelledInfluenza A viruses (IAVs) are maintained mainly in wild birds, and despite frequent spillover infections of avian IAVs into mammals, only a small number of viruses have become established in mammalian hosts. A new H3N2 canine influenza virus (CIV) of avian origin emerged in Asia in the mid-2000s and is now circulating in dog populations of China and South Korea, and possibly in Thailand. The emergence of CIV provides new opportunities for zoonotic infections and interspecies transmission. We examined 14,764 complete IAV genomes together with all CIV genomes publicly available since its first isolation until 2013. We show that CIV may have originated as early as 1999 as a result of segment reassortment among Eurasian and North American avian IAV lineages. We also identified amino acid changes that might have played a role in CIV emergence, some of which have not been previously identified in other cross-species jumps. CIV evolves at a lower rate than H3N2 human influenza viruses do, and viral phylogenies exhibit geographical structure compatible with high levels of local transmission. We detected multiple intrasubtypic and heterosubtypic reassortment events, including the acquisition of the NS segment of an H5N1 avian influenza virus that had previously been overlooked. In sum, our results provide insight into the adaptive changes required by avian viruses to establish themselves in mammals and also highlight the potential role of dogs to act as intermediate hosts in which viruses with zoonotic and/or pandemic potential could originate, particularly with an estimated dog population of ∼ 700 million.ImportanceInfluenza A viruses circulate in humans and animals. This multihost ecology has important implications, as past pandemics were caused by IAVs carrying gene segments of both human and animal origin. Adaptive evolution is central to cross-species jumps, and this is why understanding the evolutionary processes that shape influenza A virus genomes is key to elucidating the mechanisms underpinning viral emergence. An avian-origin canine influenza virus (CIV) has recently emerged in dogs and is spreading in Asia. We reconstructed the evolutionary history of CIV and show that it originated from both Eurasian and North American avian lineages. We also identified the mutations that might have been responsible for the cross-species jump. Finally, we provide evidence of multiple reassortment events between CIV and other influenza viruses (including an H5N1 avian virus). This is a cause for concern, as there is a large global dog population to which humans are highly exposed.

Dataset Information

Characterization and Evolutionary Analysis of a Novel H3N2 Influenza A Virus Glycosylation Motif in Southern China.

Publications

Characterization and Evolutionary Analysis of a Novel H3N2 Influenza A Virus Glycosylation Motif in Southern China.

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