Taha Y. Taha

The paper tracks SARS-CoV-2 mutations over 90 days in an HIV-positive individual and tests their functional impact on viral entry and replication.

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.

This study identifies multiple dispersed packaging signals in the SARS-CoV-2 genome that cooperate to direct RNA packaging into virions, revealing a dynamic mechanism for coronavirus genome assembly.

The paper links protease sequence variation to biochemical parameters and viral fitness using high-throughput enzymology and replication assays.

This paper identifies AVI-6451, an orally bioavailable inhibitor of SARS-CoV-2 Mac1 with once-daily efficacy in a mouse model.

This study identifies the non-spike R204P mutation in the SARS-CoV-2 Omicron XEC variant as a driver of increased inflammation and pathogenicity through NF-κB activation.

This study identifies Mac1 as a therapeutic target for SARS-CoV-2 and demonstrates that AVI-4206, a small molecule inhibitor, reduces viral replication and improves survival in an animal model.

This paper describes the discovery of new coronavirus MPro inhibitors with improved pharmacokinetics, broad-spectrum antiviral activity, and superior in vivo efficacy compared to existing drugs.

This study identifies the L260F mutation in NSP6 as enhancing RNA replication and pathogenesis in recent SARS-CoV-2 variants, independent of Spike function.

The paper resolves the x-ray structure of SARS-CoV and SARS-CoV-2 SUD-N/M domains and shows they have rotational flexibility, with disulfide bonds absent in pangolin-SARS and related viruses.

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.