Fanchong Jian

This study shows that the lack of ancestral SARS-CoV-2 immune imprinting in children makes them more susceptible to BA.3.2.2 infection, as it evades neutralizing antibodies typically present in adults.

The paper shows that the SARS-CoV-2 variant PJ.2.1 has high ACE2-binding capability but limited immune evasion, suggesting structural changes that may enable future immune escape.

This study evaluates the antibody evasion and receptor binding of SARS-CoV-2 variants PQ.16.1.1 and RK.1, finding reduced ACE2 engagement but increased immune evasion.

This study identifies a hierarchical activation threshold in RSV F antibody repertoires, explaining pediatric vulnerability and adult protection through distinct antibody subclasses and epitope targeting.

This study shows that V(D)J-humanized mice can replicate severe SARS-CoV-2 immune imprinting in humans, revealing that pre-existing antibody abundance influences imprinting severity.

The paper isolates human monoclonal antibodies against SFTSV Gn, identifies four neutralizing epitope groups, and validates their neutralization through structural analysis.

DeepCoV predicts SARS-CoV-2 variant dominance and evolution using DMS data and epidemiological surveillance, achieving high accuracy and capturing spatiotemporal dynamics.

This paper predicts SARS-CoV-2 RBD evolution using deep mutational scanning to identify broadly neutralizing antibodies effective against existing and prospective variants.

SARS-CoV-2 variant BA.3.2 strongly evades neutralizing antibodies but exhibits low infectivity due to a closed spike conformation, whereas NB.1.8.1 combines high ACE2 affinity with humoral immune escape.

The paper analyzes virological and antigenic traits of SARS-CoV-2 variants LF.7.2.1, NP.1, and LP.8.1, finding trade-offs between immune evasion and ACE2 binding efficiency.

The paper introduces two new methods, ChrODIE and ANDIE, for mapping chromatin accessibility and histone modifications without enzymatic cleavage, enabling multi-omics integration.

The paper introduces a method to map transcription factor binding sites genome-wide with single-base resolution and applies it to study cell-type-specific TF cooperativity in human tissues.

This study investigates the structural and molecular basis of enhanced ACE2 binding in SARS-CoV-2 KP.3 variant through Cryo-EM and MD simulations, revealing synergistic mutational effects.

This study shows that SARS-CoV-2 variants KP.3.1.1 and XEC have enhanced immune evasion through NTD glycosylation, despite maintaining high ACE2 binding and infectivity.

This study analyzes the humoral immune response to SARS-CoV-2 XBB and JN.1 lineages, showing JN.1 elicits superior neutralization and highlights the need for JN.1-based vaccine boosters.

The paper investigates how Omicron-specific naive B cell maturation after breakthrough infection alleviates immune imprinting from inactivated SARS-CoV-2 vaccines.

This study identifies ultra-potent Omicron-specific antibodies targeting the N1/N2 loop of the Spike NTD, which neutralize SARS-CoV-2 by competing with ACE2 and blocking S1 shedding, but are evaded by BA.2.86 and BA.2.87.1 sublineages.

This study investigates how N354 glycosylation in the SARS-CoV-2 spike protein affects viral fitness and human adaptation through multiple mechanisms.

The paper compares SARS-CoV-2 variants from China and other countries, finding that Chinese variants have more dispersed RBD mutations with higher ACE2 binding and less immune evasion potential due to a distinct immune background.

This study assesses the antigenic properties and immune evasion of the SARS-CoV-2 variant BA.2.87.1, finding it less resistant to neutralizing antibodies than JN.1 but with compensatory deletions in the NTD.

The paper analyzes antibody neutralization data from multiple countries to assess how prior exposure to SARS-CoV-2 variants affects neutralization profiles of BA.2.86 and its descendants.

This study shows that convergent evolution of SARS-CoV-2 XBB lineages at RBD positions 455-456 synergistically enhances antibody evasion and ACE2 binding through epistatic interactions.

The paper shows JN.1 outcompetes BA.2.86 and other variants by evading antibodies more effectively, despite reduced ACE2 binding.

This study characterizes the antigenic properties and infectivity of the SARS-CoV-2 BA.2.86 variant, finding it evades immune responses but has reduced infectivity compared to previous variants.