Simon Alexander Mallal

This study longitudinally tracks antigen-specific T cells in human upper airway tissues and blood, finding sustained memory T cell populations over 18 months.

The paper identifies keystone organisms by analyzing immunological traits and clinical emergence patterns, finding herpesviruses and Mycobacterium tuberculosis as key pathogens with broad niche and immune breadth.

This study identifies CD4+ T cell epitopes in chronic chikungunya virus disease, revealing conserved epitopes across alphaviruses and providing tools for T cell response analysis.

The paper identifies adaptive-like NK cells in influenza responses linked to humoral immunity and influenced by age and sex, suggesting potential vaccine strategies for aging populations.

This study identifies genetic risk factors for tuberculosis in Brazil using GWAS and single-cell transcriptomics, finding SNPs associated with gene expression in multiple cell types.

The paper identifies PINK1 as an autoantigen targeted by T cells in Parkinson's disease, with reactivity predominantly observed in male patients.

This study examines cytokine and chemokine receptor expression in adipose tissue endothelial cells of HIV-positive individuals, identifying receptor differences and their potential role in vascular dysfunction.

This study links early SARS-CoV-2 viral load in nasal samples to mucosal gene expression patterns associated with immune signaling and response in symptomatic adults.

Periscope identifies and quantifies sub-genomic RNAs in SARS-CoV-2 genomic data, detecting canonical and non-canonical sgRNAs with high fidelity.

The paper shows that B.1.1.7 SARS-CoV-2 lineage has increased subgenomic RNA expression compared to other lineages, with a noncanonical sgRNA near ORF9b showing a 16-fold increase in median expression.

Single-cell RNA-sequencing identifies distinct epithelial and mesenchymal cell types and their roles in pulmonary fibrosis.

The paper identifies Rif1 as a regulator of replication fork progression in Drosophila, acting downstream of SUUR to inhibit fork progression and control DNA copy number.