Increasing appearance of reassortant influenza B virus in Taiwan from 2002 to 2005

Genetic and antigenic analyses of influenza B virus field strains isolated in Taiwan from 1998 to 2005 were performed. To investigate the molecular evolution of influenza B viruses, sequence analysis of the hemagglutinin (HA1 subunit) and neuraminidase genes was performed. All influenza B viruses isolated between 1998 and 2000 belonged to the B/Yamagata/16/88 lineage. The B/Victoria/2/87 lineage, which was cocirculating with the Yamagata lineage, was identified in Taiwan in March 2001. Concurrently, there was an increasing prevalence of this lineage in many parts of the world, including North America and Europe, during the 2001-2002 season. Since 2002, genetic reassortants of influenza B virus with the Victoria lineage of hemagglutinin and the Yamagata lineage of neuraminidase have been found at a rate of 46%. Therefore, in 2002, at least three sublineages of influenza B virus strains, the B/Shanghai/361/2002-like strain (Yamagata lineage), the B/Hong Kong/330/01-like strain (Victoria lineage), and the B/Hong Kong/1351/02-like strain (B reassortant lineage), were identified in Taiwan. The results showed that genetically distinct lineages can cocirculate in the population and that the reassortment among these strains plays a role in generating the genetic diversity of influenza B viruses. Interestingly, from January to April 2005, B reassortant viruses became dominant (73%) in Taiwan, which indicated that a mismatch had occurred between the influenza B vaccine strain recommended for the 2004-2005 season in the Northern hemisphere by the World Health Organization and the epidemic strain.     

Cocirculation and evolution of two lineages of influenza B viruses in europe and Israel in the 2001-2002 season

Forty-nine influenza B virus isolates collected in Belgium, Finland, Spain, and Israel during the 2001-2002 winter season were categorized into either of two lineages, B/Yamagata/16/88 or B/Victoria/2/87, based on the phylogenetic studies of HA1 sequences. The data trace the geographic spread of B/Victoria/2/87-like viruses and support the emergence of B/Hong Kong/1351/02-like viruses, possibly due to selective advantages of reassortment.     

Molecular characterization of influenza B viruses circulating in northern Italy during the 2001-2002 epidemic season

During the 2001-2002 influenza season, virological surveillance highlighted the predominant circulation of B viruses (86% of isolates) in Italy, in contrast to many other countries in Europe and North America where AH3N2 viruses were isolated most frequently, and in contrast to the infrequent isolation of B viruses in Italy during the previous two years. Associated with this predominance of influenza B was the re-emergence of B/Victoria/2/87-lineage viruses, closely related to B viruses prevalent during the 1980s, which are distinct antigenically and genetically from circulating B/Sichuan/379/99-like viruses of the B/Yamagata/16/88 lineage, which predominated in most parts of the world during the last 10 years. Ninety-four viruses isolated in two regions of northern Italy were characterized, 50 by direct sequencing of haemagglutinin (HA). Viruses of both Victoria and Yamagata lineages co-circulated throughout the 12 weeks of the influenza season. The HAs of the Yamagata-lineage viruses were heterogeneous and comprised two sublineages, represented by B/Sichuan/379/99 and B/Harbin/7/94, whereas the Victoria-lineage viruses were more homogeneous and closely related to B/Hong Kong/330/01, the current prototype vaccine strain. The antigenic and genetic characteristics of the viruses correlated with certain epidemiological features. In particular, the low age (<14 years) of individuals infected with B/Hong Kong/330/01-like viruses is likely to reflect the greater susceptibility of the youngest cohort, due to lack of previous exposure to Victoria-lineage viruses, and is consistent with the conclusion that vaccination with a B/Sichuan/379/99-like virus would give poor protection against infection with B/Hong Kong/330/01-like (Victoria-lineage) viruses.     

Genetic diversity of influenza B virus: the frequent reassortment and cocirculation of the genetically distinct reassortant viruses in a community

To characterize the genetic diversity of influenza B viruses isolated during one influenza season, the antigenic and genetic relationships among 20 strains of influenza B virus isolated in February and March 2001 at one pediatric clinic in Yamagata City, Japan, were investigated. The HA gene and seven other gene segments were phylogenetically divided into three distinct sublineages (Harbin/7/94-, Tokyo/6/98-, and Shiga/T30/98-related lineage) of the Yamagata/16/88-like lineage. The NS genes of the viruses belonging to the Harbin/7/94-related lineage have additional three nucleotides at positions 439-447, and were phylogenetically distinguishable from those of the currently circulating Yamagata/16/88- and Victoria/2/87-like lineages, but were closely related to that of the Yamagata/16/88-like lineage isolated before 1994. Moreover, four strains of influenza B virus isolated in the same community between 2002 and 2003 were further examined. Phylogenetic analysis revealed that a virus of Victoria/2/87-like lineage isolated in 2003 had acquired the NA, NS, M, and PA gene segments from a Shiga/T30/98-like virus, and two strains of Harbin/7/94-related lineage had acquired the various gene segments from Shiga/T30/98-like virus through a reassortment event. These results indicate that genetically distinct multiple viruses can combine to cause an influenza B epidemic in a community and that the frequent reassortment among these viruses plays a role in generating the genetic diversity of influenza B viruses.     

Molecular analysis of isolates from influenza B outbreaks in the U.S. and Nepal, 2005

Summary. Currently circulating influenza B viruses can be divided into two antigenically and genetically distinct lineages referred to by their respective prototype strains, B/Yamagata/16/88 and B/Victoria/2/87, based on amino acid differences in the hemagglutinin surface glycoprotein. During May and July 2005, clinical specimens from two early season influenza B outbreaks in Arizona and southeastern Nepal were subjected to antigenic (hemagglutinin inhibition) and nucleotide sequence analysis of hemagglutinin (HA1), neuraminidase (NA), and NB genes. All isolates exhibited little reactivity with the B/Shanghai/361/2002 (B/Yamagata-like) vaccine strain and significantly reduced reactivity with the previous 2003/04 B/Hong Kong/330/2001 (B/Victoria-like) vaccine strain. The majority of isolates were antigenically similar to B/Hawaii/33/2004, a B/Victoria-like reference strain. Sequence analysis indicated that 33 of 34 isolates contained B/Victoria-like HA and B/Yamagata-like NA and NB proteins. Thus, these outbreak isolates are both antigenically and genetically distinct from the current Northern Hemisphere vaccine virus strain as well as the previous 2003–04 B/Hong Kong/330/2001 (B/Victoria lineage) vaccine virus strain but are genetically similar to B/Malaysia/2506/2004, the vaccine strain proposed for the coming seasons in the Northern and Southern Hemispheres. Since these influenza B outbreaks occurred in two very distant geographical locations, these viruses may continue to circulate during the 2006 season, underscoring the importance of rapid molecular monitoring of HA, NA and NB for drift and reassortment.     

Internal epidemic influenza virus proteins: isolation and investigation

The internal influenza virus proteins M1 and RNP free from surface protein impurities were isolated from subviral particles (virions free from HA and NA ectomenes). The spikeless particles had no propensity to aggregate in the solution at pH 5.0 as compared with native viruses. The subviral particles of B/Hong Kong/330/01 influenza virus, which belonged to B/Victoria/2/87-lineage, were obtained by proteolytic treatment with the enzyme bromelain under the same conditions as in cases of influenza B viruses of B/Jamagata/16/88 lineage. A chromatographic analysis of the tryptic hydrolyzates obtained for matrix (M1) proteins of A(H1N1) and A(H3N2) influenza viruses revealed differences that were greatest between the protein M1 molecules isolated from influenza viruses of different subtypes of hemagglutinine. These findings suggest there are variations in the structure of this conservative internal viral protein M1 during evolution.     

Cocirculation of two distinct evolutionary lineages of influenza type B virus since 1983

During 1988-1989 two highly distinct antigenic variants of influenza type B were recognized in hemagglutination-inhibition tests with postinfection ferret serum. These viruses were antigenically related to either B/Victoria/2/87, the most recent reference strain, or B/Yamagata/16/88, a variant that was isolated in Japan in May 1988. All influenza B viruses isolated in the United States during an epidemic in the winter of 1988-1989 were antigenically related to B/Victoria/2/87. However, in several countries in Asia, both B/Victoria/2/87-like viruses and B/Yamagata/16/88-like viruses were isolated. Sequence analysis of the hemagglutinin (HA) genes of several influenza B isolates from 1987 to 1988 indicated that the HA1 domains of the B/Yamagata/16/88-like viruses and B/VI/87-like viruses isolated in 1988 differed by 27 amino acids. Evolutionary relationships based on this sequence data indicated that the B/Yamagata/16/88-like viruses were more closely related to epidemic viruses from 1983 (B/USSR/100/83-like viruses) than to more recent reference strains such as B/Victoria/2/87. All other Asian strains, as well as selected isolates from the United States in 1988, were confirmed by sequence analysis as being genetically related to B/Victoria/2/87. These data provide clear evidence that two parallel evolutionary pathways of influenza type B have existed since at least 1983 and that viruses from each of the separate lineages were isolated from cases of influenza B in 1988. This finding is similar to earlier observations for type A H1N1 and H3N2 influenza viruses.     

Changes in the hemagglutinins and neuraminidases of human influenza B viruses isolated in Italy during the 2001-02, 2002-03, and 2003-04 seasons

Throughout most of the last decade, B/Yamagata/16/88-lineage influenza viruses were predominant among the B isolates circulating worldwide, whereas B/Victoria/2/87-lineage viruses were isolated infrequently and restricted geographically to eastern Asia. During the 2001-02 influenza season, B/Victoria/2/87-lineage viruses re-emerged in North America and Europe and spread worldwide. Virological surveillance in Italy during that season showed wide circulation of influenza B viruses, of which most were antigenically related to the B/Sichuan/379/99 (Yamagata-lineage) vaccine strain, together with a smaller number of B viruses antigenically similar to B/HongKong/330/01, a recent B/Victoria/2/87-lineage antigenic variant. In the subsequent 2002-03 epidemic season, B viruses with a Victoria-lineage hemagglutinin (HA), more closely related to that of B/Shandong/7/97, were isolated exclusively. Similar strains have continued to predominate among the few B viruses isolated in Italy during last season (2003-04), although most influenza B viruses, isolated sporadically elsewhere in Europe, again belong to the Yamagata-lineage. In the present study, phylogenetic analyses of the HA and neuraminidase (NA) genes of representative B strains, isolated throughout Italy during 2001-04, showed that during the first influenza season the NA genes, as well as the HA genes, separated into the two distinct clades, the Yamagata- and Victoria-lineages, and showed no evidence of genetic reassortment. On the contrary, all the B viruses isolated in the 2002-03 and most of those isolated in the 2003-04 epidemic season were "Victoria HA-Yamagata NA" reassortants similar to those isolated in other parts of the world, showing that these reassortants became established in the human population. The frequency of reassortment between HA and NA of distinct lineages and sublineages highlights again the importance of detailed molecular analyses of both surface glycoproteins in understanding the evolution of influenza B viruses.     

Genetic analysis and evaluation of the reassortment of influenza B viruses isolated in Taiwan during the 2004-2005 and 2006-2007 epidemics

Influenza B viruses were predominant in Taiwan during the 2004-2005 epidemic and both Victoria and Yamagata lineage viruses co-circulated. A reassortant influenza B virus that contained a Victoria lineage hemagglutinin (HA) gene and Yamagata lineage neuraminidase (NA) gene appeared first in 2002 and became predominant during the 2004-2005 epidemic. During the 2006-2007 epidemic, an influenza B outbreak occurred in Taiwan and only Victoria lineage viruses circulated. We characterized the viruses isolated in the 2006-2007 epidemic and found that the HA genes of influenza B viruses from that epidemic were highly similar to those from the 2004-2005 epidemic. We also analyzed the NA genes of isolates from the 2006-2007 epidemic and found that they all belonged to the Yamagata lineage and formed a new genetic subclade. Comparison of isolates from the 2004-2005 and 2006-2007 epidemics revealed four substitutions, N220K, E320D, K343R and E404K in NA genes. Although the HA sequences from the 2006-2007 epidemic were similar to those from the 2004-2005 epidemic, the NA sequences differed, suggesting distinct patterns of evolution of the HA and NA genes from 2004-2007 in Taiwan. This study emphasizes that the evolution of the NA genes may contribute to reemergence of influenza B viruses.     

Antigenic and genetic analyses of influenza B viruses\\ isolated in Lusaka, Zambia in 1999

Summary.  Previous studies of the hemagglutinin (HA) genes of various influenza B virus isolates demonstrated the existence of two antigenically distinct virus lineages represented by B/Victoria/2/87 and B/Yamagata/16/88, respectively. Here, we investigated the antigenic and genetic characteristics of influenza B viruses isolated from children living in Lusaka, Zambia between January and May 1999. Antigenic analysis with chicken antiviral sera showed that all the Zambian isolates had the HA protein belonging to B/Yamagata/16/88-related lineage. Furthermore, phylogenetic analyses of the eight RNA segments performed by using the total or partial nucleotide sequences of the two representative Zambian strains (B/Lusaka/270/99 and B/Lusaka/432/99) as well as the previously reported sequences suggested that the Zambian viruses are closely related to the recently circulating reassortants represented by B/Shiga/T30/98 and B/Yamanashi/166/98 which acquired the genes coding for three polymerase proteins (PB2, PB1, and PA), HA, nucleoprotein, and matrix protein from a B/Yamagata/16/88-like parent and the gene encoding nonstructural proteins (NS1 and NS2) from a B/Guandong/8/93-like parent. Accepted June 15, 2001 Received April 17, 2001     

Influenza viruses which preconditioned the epidemic rise in Russia in 2002-2003. A resumed circulation of influenza viruses similar to V/Victoria/2/87

According to research, the epidemic rise of influenza was preconditioned, during 2002-2003, in Russia by the circulation of influenza A(H1N1), A(H3N2) and B viruses. The Center of Influenza Ecology and Epidemiology undertook a study of 178 epidemic strains: 41 strains A(H1N1), 116 strains A(H3N2) and 21 strains of influenza B were among them. All strains were isolated in the MDCK cell culture. A simultaneous isolation in embryonated eggs as well as changing of the isolation system from MDCK to embryonated eggs were found to be effective only for influenza A(H1N1) viruses. According to the antigenic analysis, all A(H1N1) viruses were variants of the etalon A/New Caledonia/20/99. The A(H3N2) viral strains' population was heterogeneous by its antigenic properties: among its isolates, there were variants similar to the etalons of A/Moscow/10/99 and of A/Panama/200/99 as well as strains, which weakly reacted with sera of both above etalons; possibly the latter were close to the etalon of A/Fujian/411/02. All epidemic strains of influenza B virus belonged, according to the antigenic properties of hemagglutinin, to the virus group of B/Victoria/2/87-like and were antigenic variants of the etalon of B/Hong Kong/22/01. This confirmed that influenza B viruses with the antigenic hemagglutinin structure of the virus group of B/Victoria/2/87-like, which were not present in Russia for more than 10 years, re-entered the active circulation. An analysis of antigenic properties of neuraminidases (NA) of the mentioned epidemic strains showed their different degrees of relationship with the NA etalons of both evolutionary groups, i.e. B/Victoria/2/87 and B/Yamagata/16/88-like. A study of paired sera obtained from patients showed a growth of antibodies to the etalons of influenza A(H1N1), A(H3N2) and B viruses of the season in question, which confirmed the virology data.     

Reassortment and evolution of current human influenza A and B viruses

During the 2001-2002 influenza season, human influenza A (H1N2) reassortant viruses were detected globally. The hemagglutinin (HA) of these H1N2 viruses was similar to that of the A/New Caledonia/20/99 (H1N1) vaccine strain both antigenically and genetically, while their neuraminidase (NA) was antigenically and genetically related to that of recent human influenza H3N2 reference viruses such as A/Moscow/10/99. All six internal genes of the H1N2 reassortants originated from an H3N2 virus. After being detected only in eastern Asia during the past 10 years, Influenza B/Victoria/2/87 lineage viruses reappeared in many countries outside of Asia in 2001. Additionally, reassortant influenza B viruses possessing an HA similar to that of B/Shandong/7/97, a recent B/Victoria/2/87 lineage reference strain, and an NA closely related to that of B/Sichuan/379/99, a recent B/Yamagata/16/88 lineage reference strain, were isolated globally and became the predominant influenza B epidemic strain. The current influenza vaccine is expected to provide good protection against H1N2 viruses because it contains A/New Caledonia/20/99 (H1N1) and A/Panama/2007/99 (H3N2) like viruses whose H1 HA or N2 NA are antigenically similar to those of recent circulating H1N2 viruses. On the other hand, widespread circulation of influenza B Victoria lineage viruses required inclusion of a strain from this lineage in influenza vaccines for the 2002-2003 season.     

The properties of the epidemic influenza viruses A and B strains circulating in Russia in the 2004-2005 epidemic season

The epidemic upsurge of influenza morbidity in Russia in 2004-2005 was caused by the active circulation of influenza A(H3N2) and B viruses. A hundred and sixty-six epidemic strains were studied. All the strains were isolated in the MCK cell culture. Influenza A(H3N2) viruses (n=77) were antigenic variants of the reference A/Fujian/411/ 2002 and A/California/7/2004 strains. Three influenza A(H1N1) viral strains that were antigenic variants of A/New Caledonia/20/99 strains were isolated in sporadic cases. Influenza B virus strains (n=83) were antigenic variants of the reference B/Shanghai/361/02--lineage B/Yamagata/l6/88. In addition, 3 antigenic variants of B/Hong Kong/ 330/2002 (lineage B/Victoria/2/87) strains were isolated. Nine (20%) strains resistant to rimantadine at a concentration of 5 microg/ml were identified. Chromatographic analysis of B/Shanghai/361/02 and BIHong Kong/330/01 viral protein M1 trypsin hydrolysates revealed differences in the profiles of chromatograms of influenza A virus proteins M1. Examination of 121 pair sera from patients revealed an increase in antibodies to influenza A(H3N2) viruses in 10-21% of cases and to influenza B viruses in 20-36% of cases.     

Genetic characterization of the hemagglutinin of two strains of influenza B virus co-circulated in Taiwan.

Two isolates of influenza B virus were obtained in the spring of 1997. One strain, B/Taiwan/21706/97, was isolated from a patient who had acute tonsillitis. The other, B/Taiwan/3143/97, was isolated from a patient who was diagnosed with meningoencephalitis. This implies that the influenza B viruses not only cause respiratory symptoms but may also cause inflammation of the nervous system. Sequence analysis of the hemagglutinin (HA) gene, HA1 domain, indicated that there were remarkable amino acid changes in the strain B/Taiwan/3143/97 compared to B/Victoria/2/87, B/Yamagata/16/88, and B/Taiwan/7/88. The changes in the positions 116, 200, 238, 242, and 271 were correlated with receptor binding. Furthermore, a potential glycosylation site at position 233 was lost. In total, 30 amino acid changes were noted at positions ranging from 116 to 295. These changes may affect the antigenicity of the virus. Phylogenetic analyses also showed that the B/Taiwan/3143/97 was located in an independent lineage, when compared to the reference strains belonging to B/Victoria/2/87 and B/Yamagata/16/88 lineages. This supports the hypothesis that influenza B viruses with distinct genetic characteristic were co-circulated in Taiwan.     

2004-2005年中国B型流感病毒抗原性及基因特性研究

目的 阐明2004-2005年中国流行的B型流感病毒血凝素抗原性及其基因变异情况.方法 对2004-2005年分离的B型毒株先进行单向血凝抑制试验;在此基础上选取不同时间、地点的B型流感毒株进行血凝素基因HA1区核苷酸序列测定并推导出其氨基酸序列,然后进行基因进化特性分析.结果 2004-2005年我国人群中同时流行着B型Yamagata系和Victoria系毒株.Yamagata系毒株与B/Shanghai/361/02比较,2004年有3.7%病毒单向血凝抑制效价有4倍以上差异,2005年有4.5%病毒单向血凝抑制效价有4倍以上差异,并且在血凝素基因HA1区发生9个氨基酸替换,在196为增加一个糖基化位点.Victoria系毒株与B/Hong kong/330/01比较,2004年有8.5%病毒单向血凝抑制效价有4倍以上差异,2005年有20.6%病毒单向血凝抑制效价有4倍以上差异,并且在HA1区发生9个氨基酸替换,在197位增加一个糖基化位点.结论 2004-2005年我国人群中流行的B型流感病毒的抗原性与B/Shanghai/361/02、B/Hong kong/330/01相比抗原性已经发生了变化.     

Evolutionary characteristics of influenza B virus since its first isolation in 1940: dynamic circulation of deletion and insertion mechanism

Summary.  New antigenic variants of B/Yamagata/16/88-like lineage which appeared in the season of 1997 as a minor strain tended to predominate in the following season. Also, we could observe for the first time, three peaks of activity caused by H3N2 virus and two variants of B influenza virus. Antigenic and phylogenetic analyses revealed that B/Victoria/2/87-like variants appeared again in Japan in 1997 after a nine-year absence. Influenza B viruses evolved into three major lineages, including the earliest strain (I), B/Yamagata/16/88-like variants (II), which comprised of three sublineages (II-(i), II-(ii), II-(iii)), and B/Victoria/2/87-like variants (III). Evolution of influenza B virus hemagglutinin was apparently distinguishable from that of influenza A virus, showing a systematic mechanism of nucleotide deletion and insertion. This phenomenon was observed to be closely related to evolutionary pathways of I, II-(i), II-(ii), II-(iii) and III lineages. It was noteworthy to reveal that the nucleotide deletion and insertion mechanism of influenza B virus completed one cycle over a fifty-year period, and that a three nucleotide deletion was again observed in 1997 strains belonging to lineage II-( iii). It was evident that amino acid substitutions accompanying nucleotide insertions were highly conserved. Received December 4, 1997 Accepted March 10, 1998     

Clinical and genetic characterization of severe influenza B-associated diseases during an outbreak in Taiwan.

BACKGROUND: Mismatches between circulating and vaccine strains of influenza virus had been observed in Taiwan. A comprehensive clinical and genetic analysis of influenza B viruses-associated important diseases was lacking. OBJECTIVES: Clinical and phylogenetic analysis of influenza B viruses during an outbreak in Taiwan. STUDY DESIGNS: Clinical manifestations of hospitalized, culture-confirmed patients were analyzed from July 2004 to June 2005. Partial genome sequence analysis of hemagglutinin (HA), neuraminidase (NA), and nonstructural (NS) genes were performed in 54 influenza B isolates during the study period, and nine srandomly chosen isolates during 2000 and 2003. RESULTS: Three specific diseases were found in these patients, including 13 of encephalitis/encephalopathy, 28 of influenza-associated myositis (IAM), and one of acute respiratory distress syndrome (ARDS). Three phylogenetic groups were identified, including reassortant strains-group 1 (Victoria lineage of HA, Yamagata lineage of NA, clade A of NS), group 2 (Yamagata lineage of HA, Yamagata lineage of NA, clade A of NS), and group 3 (Yamagata lineage of HA, Yamagata lineage of NA, clade B of NS). CONCLUSIONS: Severe influenza B-associated disease in children was not rare and might be fatal. We offered the evidence of co-circulation of the two HA lineages in the same outbreak.     

Phylogenetic Analysis of Neuraminidase Gene of H9N2 Influenza Viruses Prevalent in Chickens in China during 1995–2002

The neuraminidase (NA) genes of 12 H9N2 influenza virus strains isolated from diseased chickens in different farms in mainland China during 1995–2002 were amplified and sequenced. Amino acids at hemadsorbing (HB) site of these isolates are different from those of A/quail/Hong Kong/G1/97-like viruses and A/chicken/Korea/96-like viruses. Neuraminidases of the 12 strains had a deletion of 3 amino acid residues at positions 63–65 as compared to that of A/turkey/Wisconsin/189/66, while those of Korea and Pakistan H9N2 isolates had no deletion. Phylogenetic analyses showed NA gene of these isolates belonged to that of A/duck/Hong Kong/Y280/97-like virus lineage. NA gene of the H9N2 viruses isolated in Korea and Pakistan belonged to lineage different from those of the 12 isolates. The present results indicate that the NA of H9N2 strains isolated in mainland China during the past 8 years were well preserved and the geographical distribution play a significant role in the evolution of the H9N2 influenza viruses.     

Recent changes among human influenza viruses

Recurrent epidemics of influenza are due to the frequent emergence of antigenic variants. With co-circulation of two influenza A subtypes and two antigenically distinct lineages of B viruses, genetic reassortment also has an important role in antigenic drift, as illustrated by recent changes in both A and B viruses. The H1N2 subtype viruses, which emerged during 2001, possessed a H1 HA similar to those of contemporary A/New Caledonia/20/99 (H1N1)-like viruses and seven genes closely related to those of recent H3N2 viruses, and did not represent a significant increase in the antigenic diversity of circulating viruses. The re-emergence of B/Victoria/2/87-lineage viruses, previously prevalent during the 1980s, in 2000 has been followed by the predominant circulation of reassortant B viruses possessing a B/Victoria-lineage HA and a B/Yamagata-lineage NA similar in sequence to those of recent B/Sichuan/379/99-like viruses. These events emphasize not only the lack of divergence in the complementary functional characteristics of the HA and NA of divergent influenza B lineages, but also the apparent convergence in compatibility between the H1 and N2 components of the two influenza A subtypes.     

Cross-reactive antibodies induced by a monovalent influenza B virus vaccine.

Influenza viruses related to the markedly antigenically divergent strains B/Yamagata/16/88 and B/Victoria/2/87 are circulating in human populations. Adults develop cross-reacting antibodies against recent and earlier influenza B virus strains after vaccination with B/Yamagata/16/88, probably because of previous influenza B virus infections or immunizations. Vaccines containing B/Yamagata/16/88 should adequately protect adults against B/Victoria/2/87 infections.