The DOI matches its Crossref record; 33 of the 33 references it cites were found in a registry or an index.
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 [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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Highly Conserved Protective Epitopes on Influenza B Viruses
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Influenza A Virus Cell Entry, Replication, Virion Assembly and Movement
Dou, D., Revol, R., Østbye, H., Wang, H., & Daniels, R. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.01581 · Cited by 621
Metadata
- 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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