Amy K. Barczak

This study examines immune responses in adults with COVID-19 who received or did not receive nirmatrelvir-ritonavir, finding no differences in immune markers between those with and without virologic rebound.

This study uses a mouse model of TB infection to investigate fibrosis mechanisms, finding persistent inflammatory macrophages and elevated matrix remodeling enzymes during treatment.

The paper models viral rebound after nirmatrelvir-ritonavir treatment, finding that target cell preservation and incomplete viral clearance drive rebound, with extended treatment reducing this risk.