Stanley M. Perlman

This paper develops a recombinant SARS-CoV-2 virus expressing reporter genes to track viral infection in wild-type mice, showing it can be used for vaccine and antiviral research without needing transgenic models.

This study uses longitudinal single-cell RNA sequencing to show that myeloid cells contribute to sustained neuroinflammation in neuroPASC, with microglia playing a central role.

This study shows that Nsp6 of β-coronaviruses remodels ER membranes and sequesters host translocation machinery into DMVs to support viral replication.

This study shows SAMHD1 promotes SARS-CoV-2 infection in lung epithelial cells by enhancing ACE2 expression through HNF1 and HNF1β, independent of its IFN-suppressive function.

This study shows IL-13 protects airway epithelial cells from SARS-CoV-2 infection in vitro but worsens disease severity in mice through eicosanoid signaling.

This study identifies pulmonary complement activation in a mouse model of severe COVID-19, showing local complement production and its role in lung injury.

This study shows SARS-CoV-2 infection causes greater metabolic disturbance in peripheral lung tissue than central tissue, despite higher viral loads in the center.

The study analyzes MERS-CoV genetic diversity in Saudi Arabian dromedary camels and humans, identifying new variants with unique Spike protein polymorphisms.

This study shows that antiviral drugs fail to prevent neurological deficits in SARS-CoV-2-infected mice, which resemble neurodegenerative diseases due to chronic inflammation.

This study uses deep mutational scanning to analyze the SARS-CoV-2 spike fusion peptide, identifying mutations affecting viral entry and antibody resistance.

This study identifies S2 domain mutations in SARS-CoV-2 spike that reduce binding to antibodies, showing antigenic drift in this region and its impact on vaccine efficacy.