Cocirculation and Evolution of Two Lineages of Influenza B Viruses in Europe and Israel in the 2001-2002 Season

Sherry, X.; Bolar, Trentice V.; Zhao, Ping; Rappaport, Ruth; Cheng, Sheau-Mei

doi:10.1128/jcm.41.12.5770-5773.2003

Cited by 46 publications

(38 citation statements)

References 15 publications

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“…The Victoria and Yamagata lineages were first detected during the 1988-1989 influenza season, and they cocirculated worldwide from 1983 to 1990 (1,(4)(5)(6). In the 1990s, the Victoria lineage became less frequently isolated and was mainly restricted to East Asia (14,15). The Victoria lineage is thought to have re-emerged in North America and Europe and spread worldwide around 2000 to 2002 (9,14,15).…”

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“…In the 1990s, the Victoria lineage became less frequently isolated and was mainly restricted to East Asia (14,15). The Victoria lineage is thought to have re-emerged in North America and Europe and spread worldwide around 2000 to 2002 (9,14,15). In China, both the Victoria and Yamagata lineages have been cocirculating for a substantial period of time (16)(17)(18)(19)(20), with more frequent dominance of the Yamagata lineage in the 1990s, especially in northern China (21,22).…”

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confidence: 99%

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Differing Epidemiological Dynamics of Influenza B Virus Lineages in Guangzhou, Southern China, 2009-2010

Tan

Guan

Lam

et al. 2013

J Virol

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The epidemiological and evolutionary dynamics of the two cocirculating lineages of influenza B virus, Victoria and Yamagata, are poorly understood, especially in tropical or subtropical areas of Southeast Asia. We performed a phylogenetic analysis of the hemagglutinin (HA) and neuraminidase (NA) sequences of influenza B viruses isolated in Guangzhou, a southern Chinese city, during 2009 to 2010 and compared the demographic and clinical features of infected patients. We identified multiple viral introductions of Victoria strains from both Chinese and international sources, which formed two phylogenetically and antigenically distinct clades (Victoria 1 and 2), some of which persisted between seasons. We identified one dominant Yamagata introduction from outside China during 2009. Our phylogenetic analysis reveals the occurrence of reassortment events among the Victoria and Yamagata lineages and also within the Victoria lineage. We found no significant difference in clinical severity by influenza B lineage, with the exceptions that (i) the Yamagata lineage infected older people than either Victoria lineage and (ii) fewer upper respiratory tract infections were caused by the Victoria 2 than the Victoria 1 clade. Overall, our study reveals the complex epidemiological dynamics of different influenza B lineages within a single geographic locality and has implications for vaccination policy in southern China.

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Differing Epidemiological Dynamics of Influenza B Virus Lineages in Guangzhou, Southern China, 2009-2010

Tan

Guan

Lam

et al. 2013

J Virol

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“…Currently, there are two major phylogenetic lineages found in circulation: B/Victoria/2/87 (B/VI) like and B/Yamagata/16/88 (B/YM) like (41,77,83). Despite the lack of subtypes, influenza B virus undergoes antigenic variation through genetic reassortment among cocirculating strains of different lineages and antigenic drift from cumulative mutations (17,48,49,56,70,83,101). Influenza B virus HAs have a mutational rate about five times slower than that observed for influenza A virus HAs (3,10,15,19,34,41,44,45,81,94,101).…”

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Crystal Structure of Unliganded Influenza B Virus Hemagglutinin

Wang

Cheng

et al. 2008

J Virol

125

141

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Here we report the crystal structure of hemagglutinin (HA) from influenza B/Hong Kong/8/73 (B/HK) virus determined to 2.8 Å. At a sequence identity of ϳ25% to influenza A virus HAs, B/HK HA shares a similar overall structure and domain organization. More than two dozen amino acid substitutions on influenza B virus HAs have been identified to cause antigenicity alteration in site-specific mutants, monoclonal antibody escape mutants, or field isolates. Mapping these substitutions on the structure of B/HK HA reveals four major epitopes, the 120 loop, the 150 loop, the 160 loop, and the 190 helix, that are located close in space to form a large, continuous antigenic site. Moreover, a systematic comparison of known HA structures across the entire influenza virus family reveals evolutionarily conserved ionizable residues at all regions along the chain and subunit interfaces. These ionizable residues are likely the structural basis for the pH dependence and sensitivity to ionic strength of influenza HA and hemagglutinin-esterase fusion proteins.Influenza virus is a negative-stranded RNA virus belonging to the Orthomyxoviridae family. Three types of influenza viruses have been detected: A, B, and C. They all have a major surface glycoprotein, hemagglutinin (HA) for influenza A and B viruses and hemagglutinin-esterase fusion (HEF) protein for influenza C virus (2,20,85,98). Infections caused by influenza A and B viruses remain a major source of human morbidity and mortality worldwide (13, 90).Influenza B virus circulates exclusively in humans and seals (66), with no subtypes. The first isolated influenza B virus strain was B/Lee/40 (44). Currently, there are two major phylogenetic lineages found in circulation: B/Victoria/2/87 (B/VI) like and B/Yamagata/16/88 (B/YM) like (41,77,83). Despite the lack of subtypes, influenza B virus undergoes antigenic variation through genetic reassortment among cocirculating strains of different lineages and antigenic drift from cumulative mutations (17,48,49,56,70,83,101). Influenza B virus HAs have a mutational rate about five times slower than that observed for influenza A virus HAs (3,10,15,19,34,41,44,45,81,94,101). The antigenic structures of influenza B virus HAs have been studied by sequence analysis of both naturally occurring variants and antibody-selected escape variants (5,6,10,35,44,45,51,76,77,94,96), using the structure of influenza A H3 HA as a reference (100). However, given the rather low sequence identity between influenza A and B virus HAs, ϳ20% for HA 1 , which is the primary target for antigenic variation, it is hard to define accurately the antigenic sites in this fashion.We have recently reported two crystal structures of influenza B/Hong Kong/8/73 virus HA (referred to as B/HK HA herein) in complex with human and avian receptor analogs (95). Comparison of these structures with those of influenza A virus HAs provided a structural basis for the receptor-binding properties of influenza A and B virus HAs and suggested the role of residue 222 (H3 numbering) as a key an...

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“…Viral RNA was extracted from influenza viruses propagated once in MDCK cells as previously described (4). HA1 fragments corresponding to nucleotides 37 to 1154 were amplified by reverse transcription-PCR using oligonucleotides 5Ј-CTATCATTGCTT TGAGCTAC (primer 1) and 5Ј-ATCTGCTGCTTGTCCTGT GC (primer 2).…”

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confidence: 99%

“…The PCR products were purified and subjected to sequencing on a genetic analyzer (ABI PRISM 3100; Applied Biosystems, Foster City, CA) with the above-mentioned oligonucleotides and two additional oligonucleotides, 5Ј-ATG CCAAACAATGACAAATT (primer 3) and 5Ј-TGTTTG GCATAGTCACGTTC (primer 4), except for group 3 specimens, for which only primers 1 and 4 were used for sequencing. Multiple alignments of the sequences were performed by the ClustalV method, and the phylogenetic tree was constructed by the neighbor-joining method using MegAlign version 5.03 (DNASTAR) as previously described (4).…”

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Molecular Evolution of Human Influenza A/H3N2 Virus in Asia and Europe from 2001 to 2003

et al. 2005

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Cocirculation and Evolution of Two Lineages of Influenza B Viruses in Europe and Israel in the 2001-2002 Season

Abstract: Forty-nine influenza B virus isolates collected in

Cited by 46 publications

References 15 publications

Differing Epidemiological Dynamics of Influenza B Virus Lineages in Guangzhou, Southern China, 2009-2010

Differing Epidemiological Dynamics of Influenza B Virus Lineages in Guangzhou, Southern China, 2009-2010

Crystal Structure of Unliganded Influenza B Virus Hemagglutinin

Molecular Evolution of Human Influenza A/H3N2 Virus in Asia and Europe from 2001 to 2003

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