Timothy W. Schacker

This study uses spatial transcriptomics to identify compartment-specific immune activation signatures in ileal and lymph node tissues of HIV-treated patients, revealing tissue-specific transcriptional differences linked to immune activation and microbial translocation.

The paper uses metabolomics to show that HIV-treated individuals have metabolic disruptions, including lipid changes and inflammation markers, despite viral suppression.

This study links microbial dysbiosis, systemic inflammation, and metabolomic disruptions to SNAE risk in treated HIV patients through multi-omic analysis.

The paper identifies HIV-producing resting T cells as the primary source of virus production in lymphoid tissue germinal centers before ART and shows their role in PANoptosis and persistence during treatment.

The paper shows HIV causes collagen deposition in lymphoid tissue early in infection, linked to TGF-β+ macrophages and HIV RNA-producing cells, suggesting early ART may not prevent fibrosis.

The paper shows that residual HIV production in lymph nodes of ART-suppressed individuals drives pyroptosis and is counter-regulated by GLP-1 upregulation in the ileum.

This study shows that pre-treatment gut microbiome diversity in HIV patients correlates with immune activation and reduced HIV RNA+ cells after N-803 treatment.

This study examines the impact of SARS-CoV-2 infection on intestinal permeability, systemic inflammation, and microbial dysbiosis in hospitalized patients, finding associations between specific microbial changes and disease severity.

The paper uses a biophysical model of the SARS-CoV-2 viral cycle to identify antiviral targets by analyzing parameter sensitivity and pairwise interactions.