ArticleVirus research2023
Identification of a GII.6 norovirus blockade antibody epitope.
Article in Virus research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Molecular Characterization of Noroviruses Causing Acute Gastroenteritis Outbreaks among US Military Recruits, 2013-2023.Emerging infectious diseases · 2024Article
- Biological and immunological characterization of major capsid protein VP1 from distinct GII.2 norovirus clusters.Scientific reports · 2024Article
- Identification of a norovirus GII-specific antigenic epitope.Archives of virology · 2024Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Noroviruses (NoVs) are the leading agent that causes acute viral gastroenteritis worldwide. Sporadic cases of GII.6 NoV have been reported primarily in addition to occasional outbreaks. Using the major capsid protein VP1 of GII.6 NoV derived from three distinct clusters, we demonstrated three blockade monoclonal antibodies (mAbs, 1F7, 1F11, and 2B6) generated previously exhibited cluster-specific binding effects. Combining sequence alignment and blocking immune epitopes, we sequentially designed a total of 18 mutant proteins containing one, two, or three mutations, or swapped regions. Indirect enzyme-linked immunosorbent assay (ELISA) demonstrated that the three blocking mAbs lost or showed significantly reduced binding for H383Y, D387N, V390D, and T391D mutant proteins. Combining data from mutant proteins with swapping regions and point mutations, the binding region of the three mAbs was mapped to residues 380-395. Sequence alignment of this region showed within-cluster conservation and between-cluster variations, further strengthening the idea of blockade epitope-mediated evolution of NoV.
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Registered trials
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