William Bolland

This study examines how SARS-CoV-2 RBD antibodies differ in function, showing that neutralizing antibodies lose effectiveness against variants but retain effector functions, while non-neutralizers remain broadly reactive but less effective overall.

This study shows that SARS-CoV-2 entry and fusion depend on cholesterol but not on ACE2 localization to lipid rafts.

This study determines the structure of HKU1-CoV receptor binding domain in complex with TMPRSS2, identifying key residues for host tropism and revealing the structural basis of TMPRSS2 activation.

This study characterizes SARS-CoV-2 variants XBB and BA.2.86/JN.1, finding they show increased fitness and antibody evasion while maintaining antiviral sensitivity.

The paper identifies a novel ACE2 isoform, LTR16A1-ACE2, induced by interferon, which is non-functional and does not enhance SARS-CoV-2 infection.