ArticleJournal of structural biology: X2026
Evolutionary and structural pathways of antibody maturation reveal principles for engineering potent SARS-CoV-2 neutralizers.
Article in Journal of structural biology: X, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The continual emergence of SARS-CoV-2 variants underscores the need to elucidate antibody maturation and apply rational design principles to optimize therapeutics. This study focused on vaccine-elicited 9C lineage, encoded by IGHV4-34, as a model for affinity maturation and structural refinement. Sequence analyses revealed strong framework conservation alongside focused diversification within CDRH3, where the invariant RWFD anchor and a recurrent SYTV block were consistently associated with potent neutralization. Phylogenetic reconstruction traced a trajectory from weakly neutralizing precursors, such as 9A91, to ultrapotent clones, like 9C2, showing nearly a 3000-fold improvement in IC₅₀ values. Computational modeling, molecular dynamics, and docking analyses demonstrated that potency arises from progressive stabilization of the CDRH3 apex, with the SYT motif at VH106-108 serving as a critical structural driver with improved IC
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.