Cocirculation of two distinct evolutionary lineages of influenza type B virus since 1983
Abstract
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.
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The time from onset to death observed with fatal influenza B was more rapid than the duration of fatal illness described for pandemic 1918 A(H1N1), pandemic 1957 A(H2N2), pandemic 1968 A(H3N2), pandemic 2009 H1N1, and seasonal A(H3N2) viruses.
“The time from onset to death observed with fatal influenza B was more rapid than the duration of fatal illness described for pandemic 1918 A(H1N1), pandemic 1957 A(H2N2), pandemic 1968 A(H3N2), pandemic 2009 H1N1, and seasonal A(H3N2) viruses [3, 10-13, 4).”
From Myocardial Injury and Bacterial Pneumonia Contribute to the Pathogenesis of Fatal Influenza B Virus Infection (2012) · cites this paper as [4]
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- Authors
- Rota, P. A., Wallis, T. R., Harmon, M. W., Rota, J. S., Kendal, A. P., & Nerome, K.
- Affiliations
- Centers for Disease Control and Prevention (US)
- National Institute of Health Sciences (JP)
- Corresponding author
- Rota, Paul A.
- Venue
- Virology
- Publisher
- Elsevier BV
- Published
- 1990-03
- Volume
- 175
- Issue
- 1
- Pages
- 59-68
- ISSN
- 0042-6822 (ISSN-L)
- OpenAlex
- W1977461039
- Cited by
- 539
- References
- 33
- Citations by year
- 2026: 14 · 2025: 23 · 2024: 22 · 2023: 18 · 2022: 31 · 2021: 32 · 2020: 36 · 2019: 40 · 2018: 41 · 2017: 23 · 2016: 31 · 2015: 30 · 2014: 29 · 2013: 30 · 2012: 14
- FWCI
- 4.47
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Virology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Influenza Virus Research Studies
- Health Sciences › Medicine › Epidemiology › Respiratory viral infections research
- Health Sciences › Medicine › Epidemiology › Virology and Viral Diseases
- Keywords
- influenza B, co-circulation, evolutionary lineages, antigenic variants, hemagglutinin gene, hemagglutination inhibition, molecular evolution
- MeSH terms
- Amino Acid Sequence, Antigens, Viral, Base Sequence, Biological Evolution, Genes, Viral, Molecular Sequence Data, Influenza B virus, Oligonucleotide Probes
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