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Substitutions near the HA receptor binding site explain the origin and major antigenic change of the B/Victoria and B/Yamagata lineages.

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Title: Substitutions near the HA receptor binding site explain the origin and major antigenic change of the B/Victoria and B/Yamagata lineages.
Authors: Rosu, Miruna E.1, Lexmond, Pascal1, Bestebroer, Theo M.1, Hauser, Blake M.2, Smith, Derek J.2, Herfst, Sander1, Fouchier, Ron A. M.1 r.fouchier@erasmusmc.nl
Source: Proceedings of the National Academy of Sciences of the United States of America. 10/18/2022, Vol. 119 Issue 42, p1-9. 9p.
Subjects: Influenza B virus, Binding sites, Recombinant viruses, Influenza viruses, Influenza A virus
Geographic Terms: Victoria
Abstract: Influenza B virus primarily infects humans, causing seasonal epidemics globally. Two antigenic variants—Victoria-like and Yamagata-like—were detected in the 1980s, of which the molecular basis of emergence is still incompletely understood. Here, the antigenic properties of a unique collection of historical virus isolates, sampled from 1962 to 2000 and passaged exclusively in mammalian cells to preserve antigenic properties, were determined with the hemagglutination inhibition assay and an antigenic map was built to quantify and visualize the divergence of the lineages. The antigenic map revealed only three distinct antigenic clusters—Early, Victoria, and Yamagata—with relatively little antigenic diversity in each cluster until 2000. Viruses with Victoria-like antigenic properties emerged around 1972 and diversified subsequently into two genetic lineages. Viruses with Yamagata-like antigenic properties evolved from one lineage and became clearly antigenically distinct from the Victoria-like viruses around 1988. Recombinant mutant viruses were tested to show that insertions and deletions (indels), as observed frequently in influenza B virus hemagglutinin, had little effect on antigenic properties. In contrast, amino-acid substitutions at positions 148, 149, 150, and 203, adjacent to the hemagglutinin receptor binding site, determined the main antigenic differences between the Early, Victoria-like, and Yamagata-like viruses. Surprisingly, substitutions at two of the four positions reverted in recent viruses of the Victoria lineage, resulting in antigenic properties similar to viruses circulating ∼50 y earlier. These data shed light on the antigenic diversification of influenza viruses and suggest there may be limits to the antigenic evolution of influenza B virus. [ABSTRACT FROM AUTHOR]
Copyright of Proceedings of the National Academy of Sciences of the United States of America is the property of National Academy of Sciences and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Substitutions near the HA receptor binding site explain the origin and major antigenic change of the B/Victoria and B/Yamagata lineages.
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  Data: <searchLink fieldCode="AR" term="%22Rosu%2C+Miruna+E%2E%22">Rosu, Miruna E.</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Lexmond%2C+Pascal%22">Lexmond, Pascal</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Bestebroer%2C+Theo+M%2E%22">Bestebroer, Theo M.</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Hauser%2C+Blake+M%2E%22">Hauser, Blake M.</searchLink><relatesTo>2</relatesTo><br /><searchLink fieldCode="AR" term="%22Smith%2C+Derek+J%2E%22">Smith, Derek J.</searchLink><relatesTo>2</relatesTo><br /><searchLink fieldCode="AR" term="%22Herfst%2C+Sander%22">Herfst, Sander</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Fouchier%2C+Ron+A%2E+M%2E%22">Fouchier, Ron A. M.</searchLink><relatesTo>1</relatesTo><i> r.fouchier@erasmusmc.nl</i>
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  Data: <searchLink fieldCode="JN" term="%22Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America%22">Proceedings of the National Academy of Sciences of the United States of America</searchLink>. 10/18/2022, Vol. 119 Issue 42, p1-9. 9p.
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  Data: <searchLink fieldCode="DE" term="%22Influenza+B+virus%22">Influenza B virus</searchLink><br /><searchLink fieldCode="DE" term="%22Binding+sites%22">Binding sites</searchLink><br /><searchLink fieldCode="DE" term="%22Recombinant+viruses%22">Recombinant viruses</searchLink><br /><searchLink fieldCode="DE" term="%22Influenza+viruses%22">Influenza viruses</searchLink><br /><searchLink fieldCode="DE" term="%22Influenza+A+virus%22">Influenza A virus</searchLink>
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  Data: <searchLink fieldCode="DE" term="%22Victoria%22">Victoria</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Influenza B virus primarily infects humans, causing seasonal epidemics globally. Two antigenic variants—Victoria-like and Yamagata-like—were detected in the 1980s, of which the molecular basis of emergence is still incompletely understood. Here, the antigenic properties of a unique collection of historical virus isolates, sampled from 1962 to 2000 and passaged exclusively in mammalian cells to preserve antigenic properties, were determined with the hemagglutination inhibition assay and an antigenic map was built to quantify and visualize the divergence of the lineages. The antigenic map revealed only three distinct antigenic clusters—Early, Victoria, and Yamagata—with relatively little antigenic diversity in each cluster until 2000. Viruses with Victoria-like antigenic properties emerged around 1972 and diversified subsequently into two genetic lineages. Viruses with Yamagata-like antigenic properties evolved from one lineage and became clearly antigenically distinct from the Victoria-like viruses around 1988. Recombinant mutant viruses were tested to show that insertions and deletions (indels), as observed frequently in influenza B virus hemagglutinin, had little effect on antigenic properties. In contrast, amino-acid substitutions at positions 148, 149, 150, and 203, adjacent to the hemagglutinin receptor binding site, determined the main antigenic differences between the Early, Victoria-like, and Yamagata-like viruses. Surprisingly, substitutions at two of the four positions reverted in recent viruses of the Victoria lineage, resulting in antigenic properties similar to viruses circulating ∼50 y earlier. These data shed light on the antigenic diversification of influenza viruses and suggest there may be limits to the antigenic evolution of influenza B virus. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
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  Data: <i>Copyright of Proceedings of the National Academy of Sciences of the United States of America is the property of National Academy of Sciences and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1073/pnas.2211616119
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        Text: English
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        Type: general
      – SubjectFull: Binding sites
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      – SubjectFull: Recombinant viruses
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      – TitleFull: Substitutions near the HA receptor binding site explain the origin and major antigenic change of the B/Victoria and B/Yamagata lineages.
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              Text: 10/18/2022
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