ArticleEmerging microbes & infections2026
Deep mutational scanning reveals the antibody escape and infectivity landscape of SARS-CoV-2 Omicron JN.1 and XEC receptor-binding domains.
Article in Emerging microbes & infections, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SARS-CoV-2 continuously accumulates mutations in the spike receptor-binding domain (RBD), affecting both viral infectivity and antibody evasion. Systematic characterization of RBD mutations is therefore essential for understanding viral adaptation under immune pressure and predicting evolutionary trajectories. In this study, we employed a two-step, non-replicating pseudovirus deep mutational scanning (DMS) platform to measure the effects of all single amino acid substitutions in the RBD of Omicron variant JN.1 and its descendant lineage XEC within a full-length spike background. To identify representative antibodies for escape profiling, we first evaluated six RBD-targeting monoclonal antibodies against JN.1 and XEC pseudoviruses. Only BD55-1205 and 719-14 sIgA retained substantial neutralizing activity and were selected for subsequent escape mapping. The results showed that most single RBD amino acid mutations did not significantly enhance pseudovirus cellular invasion. Among mutations that are functionally retaining and confer marked escape from either antibody, most high escape substitutions cluster within the receptor-binding motif (RBM) and receptor-binding ridge. Furthermore, BD55-1205 and 719-14 sIgA each exhibited distinct, antibody-specific escape sites, demonstrating that different epitope preferences exert unique selective pressures within the same viral lineage. Overall, this pseudovirus-based DMS analysis elucidates the molecular mechanisms of immune escape and fitness for the JN.1 and XEC lineages. Our findings provide critical insights for forecasting SARS-CoV-2 evolution under population immunity and offer guidance for assessing emerging variants, selecting vaccine strains, and optimizing therapeutic antibodies.
Indexed as
Identifiers
What Socratic 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 Socratic graph.