Ian A. Mellis

The paper develops a monoclonal antibody panel to track antigenic evolution of SARS-CoV-2 JN.1 subvariants and identifies differences in antibody-evasion profiles between JN.1 and BA.3.2 lineages.

This study evaluates antibody evasion and ACE2 receptor engagement of SARS-CoV-2 variant RW.1.1, finding reduced receptor binding but no increased serum resistance compared to other variants.

This study finds that young children have lower neutralizing antibody titers against BA.3.2.2 compared to adults, despite similar titers against dominant variants, suggesting age-related differences in susceptibility.

This study evaluates the effectiveness of LP.8.1-targeted mRNA vaccines in boosting neutralizing antibodies and reducing immune imprinting from ancestral SARS-CoV-2 strains.

This study evaluates VYD2311, a new monoclonal antibody, showing it neutralizes multiple SARS-CoV-2 variants more effectively than pemivibart, making it a potential candidate for immunocompromised individuals.

This study compares antibody evasion and receptor binding of SARS-CoV-2 subvariants, finding that LP.8.1.1 has high ACE2 affinity, while NB.1.8.1 and XFG show greater antibody evasion.

This study optimizes a human monoclonal antibody to enhance its neutralization of SARS-CoV-2 variants, including subvariants XEC and LP.8.1, through structural analysis and engineering.

This study assesses whether 2025 COVID-19 vaccines need updating by testing neutralizing antibody titers against emerging variants in individuals vaccinated with KP.2-based mRNA vaccines.

This study evaluates the antibody evasion of SARS-CoV-2 subvariants KP.3.1.1 and XEC compared to their parental variants, finding increased resistance to neutralization by sera and antibodies targeting the spike protein.

This study evaluates KP.2-based monovalent mRNA vaccines and finds they robustly boost neutralizing antibodies against current SARS-CoV-2 variants, including KP.3.1.1 and XEC.

This study examines how recurrent spike mutations in SARS-CoV-2 JN.1 sublineages affect immune evasion, ACE2 affinity, and infectivity, identifying growth advantages in specific sublineages.

This study shows that neutralizing antibodies against SARS-CoV-2 variants remain stable for three months after an XBB.1.5 mRNA vaccine booster.

This study compares the antibody evasion, ACE2 binding, and infectivity of SARS-CoV-2 BA.2.87.1 with EG.5.1 and JN.1, finding BA.2.87.1 has lower immune evasion and reduced infectivity.

XBB.1.5 monovalent mRNA vaccine booster significantly increases neutralizing antibodies against multiple SARS-CoV-2 variants in both uninfected and previously infected individuals.

The paper identifies molecular factors that mark pluripotency potential in rare somatic cells by analyzing fibroblast reprogramming efficiency.

The paper investigates transcriptional adaptation in mammalian cells using computational analysis, mathematical modeling, and machine learning, identifying widespread prevalence and single-cell manifestations of compensatory gene networks.

The paper investigates cell type determination during cardiac differentiation of hiPS cells, finding that cell type specification begins shortly after seeding and is cell-autonomous.

The paper shows that resistant fates in cancer cells are predetermined by intrinsic molecular differences, not microenvironmental factors, and can be influenced by drug type and dose.

The paper identifies transcription factors that maintain cell identity by analyzing their responsiveness to perturbations in human iPSC-derived cardiac myocytes and fibroblasts.

The paper uses allele-specific RNA imaging to show that allelic imbalances in tissues can result from transcriptional bursting and low mRNA abundance.

This paper introduces clampFISH, a method for detecting RNA with high-gain signal amplification, enabling single-cell and single-molecule resolution using fluorescent probes.

The paper develops an RNA FISH method to visualize adenosine-to-inosine editing in single cells and finds no correlation with nuclear localization or paraspeckle association.