Miguel Padilla‐Blanco

This study identifies how a single mutation in the Omicron variant of SARS-CoV-2's ORF3a protein alters its host-cell remodelling effects, shifting from lipid accumulation to preserving Golgi structure.

This study shows that SARS-CoV-2 ORF7a causes mitochondrial dysfunction by activating PDK4 and inhibiting complex I, altering host metabolism.

This study uses in vitro evolution to show that stringent selection pressures rapidly converge on Omicron-like mutations in SARS-CoV-2 spike protein, mirroring real-world viral evolution patterns.

This study shows that SARS-CoV-2 accessory proteins ORF3a and ORF9b suppress monocytic inflammatory responses, with Omicron variants enhancing this effect.

This paper introduces CoVFit, a protein language model that predicts SARS-CoV-2 variant fitness using spike protein sequences, identifying fitness-enhancing mutations and predicting emerging variants.

This study investigates the virological characteristics of the SARS-CoV-2 BA.2.86 variant, finding it has higher reproduction number than EG.5.1 but lower pathogenicity and replication capacity compared to BA.2.

This study investigates the virological properties of the SARS-CoV-2 JN.1 variant, focusing on its mutations and potential immune evasion capabilities.

The paper investigates the virological features of the SARS-CoV-2 EG.5.1 variant, finding its fitness and antiviral sensitivity comparable to XBB.1.5, with structural differences in spike proteins.