Sarah M. Fortune

This study uses spatial transcriptomics to identify a hypoxia-associated SPP1-enriched microenvironment in pediatric TB granulomas that may contribute to incomplete bacterial clearance.

This study identifies idsA2 mutations as a mechanism of ethambutol resistance in Mtb by showing they enhance drug resistance through metabolic remodeling.

This study uses whole genome sequencing of Mycobacterium tuberculosis in non-human primates to identify distinct mutational trajectories in SIV-co-infected and ART-treated animals, revealing differential immune pressures and mutation patterns.

This study examines drug response patterns in diverse Mycobacterium tuberculosis strains to combination therapy, finding that strain-specific sensitivity varies more than genetic distance.

This study shows that antiretroviral treatment (ART) does not prevent extrapulmonary tuberculosis in SIV/Mtb co-infected macaques, despite suppressing SIV replication.

The study shows that prior Mtb infection protects against reinfection with a genetically distinct strain in macaques, suggesting broad vaccine efficacy across Mtb lineages.

The paper identifies variants in Mycobacterium tuberculosis associated with decreased virulence gene expression and increased transmissibility, particularly in drug-resistant strains.

This study evaluates antibody responses to mosquitoes and arboviruses using a multiplexed phage display library to identify epitopes and antigens associated with exposure.

The paper identifies distinct antibody-based signatures and functionalities in latent and active pediatric tuberculosis, highlighting differences in humoral immune responses that may inform diagnostic and therapeutic strategies.

The paper investigates TB relapse in a macaque model, finding that complete sterilization protects against relapse but PET CT cannot predict it, and that Mtb dissemination originates from both lung and lymph nodes.

This study identifies protective antibodies against Mycobacterium tuberculosis and shows that their Fc-effector function and Fab domains collaborate to restrict infection through immune cell reorganization.

This study identifies Mtb genes essential for survival in vaccinated and previously infected hosts using TnSeq, revealing differences in genetic requirements across immunization strategies.

This study identifies hypoxia as a key driver of immune dysfunction in TB granulomas, correlating with bacterial persistence.

The paper shows that CD4 T cells and innate CD8+ lymphocytes are essential for IV BCG-induced protection against tuberculosis in macaques.

This paper develops an engineered Mycobacterium tuberculosis strain with kill switches for a safe TB human challenge model, showing rapid clearance and low escape rates.

The paper uses Markov Fields to integrate multi-modal immune data from vaccinated macaques, identifying critical immune interactions and predicting perturbation effects.

This study identifies beta-carboline compounds produced by vaginal lactobacilli that reduce inflammation by suppressing immune signaling pathways and demonstrate therapeutic potential in a mouse model.

The paper shows that CD4+ T cells reduce inflammation and disease severity during Mtb reinfection by reprogramming CD8+ T cells and innate immune cells.

This study uses multi-omics approaches to analyze myeloid cell diversity in TB granulomas and identifies IFN-γ, TGF-β, and time as factors driving macrophage diversity.

This study shows antibiotic treatment after primary Mtb infection reduces lung inflammation but does not eliminate protection against reinfection in macaques.

This study investigates the evolutionary adaptation of Mycobacterium tuberculosis lactate dehydrogenase (LldD2) under host pressure, showing its role in metabolic flexibility and virulence.

This study shows that mycobacterial DnaQ acts as an alternative proofreader, working with the PHP domain to maintain DNA replication fidelity and prevent mutations.

This study defines the role of RNase E in mRNA degradation in Mycolicibacterium smegmatis, showing it limits degradation of 89% of protein-coding genes and has distinct sequence preferences compared to gram-negative bacteria.