Mir Mubashir Khalid

This study shows that SARS-CoV-2's ORF8 protein reprograms macrophages to enhance viral infection of lung epithelial cells, contributing to lung pathology in COVID-19.

The paper investigates how mutations in SARS-CoV-2 M and N proteins balance viral particle assembly and immune evasion through co-evolution.

The paper identifies age-associated Th2-like CD8 memory T cells in human blood and links their accumulation to health conditions like asthma and diabetes.

The paper identifies phospholipidosis as a common artifact in antiviral drug repurposing and introduces a microplate-based assay to detect it, finding that 65% of tested drugs induce it.

This study shows ORF8 suppresses viral particle production by interacting with Spike and causing Golgi fragmentation, supporting evolutionary pressure to delete ORF8 in SARS-CoV-2 variants.

The paper shows that BET proteins are antiviral factors against SARS-CoV-2, and the viral E protein neutralizes BET-mediated post-entry antiviral effects.

This paper introduces SARSNotch, a sentinel cell system that detects SARS-CoV-2 Spike protein and triggers genetic responses in cell lines and T lymphocytes.

The paper investigates how acetylation and phosphorylation of RNA polymerase II CTD interact through RPRD proteins, showing acetylation regulates phosphorylation and vice versa.