Markus Hoffmann

The paper characterizes the epidemiology and virology of the SARS-CoV-2 variant PJ.2.1, finding it spreads mainly in older adults and shows increased ACE2 binding but not greater antibody evasion.

The paper shows how SARS-CoV-2 variants, particularly Omicron, evolved proteolytic controls at the Spike furin cleavage site to enhance transmission while reducing lower respiratory tract pathogenicity.

This study identifies mutations in the MERS-CoV S protein that reduce soluble DPP4 binding and confer resistance to sDPP4 while maintaining entry into cells with high DPP4 levels.

This study shows the QTQTX motif in BA.3.2 S protein is not required for cleavage or lung cell entry, which depends on TMPRSS2 instead.

This paper shows that SARS-CoV-2 Omicron lineages replicate using a specific ACE2 pool that does not complex with TMPRSS2, unlike pre-Omicron variants.

This paper identifies Sec61β as essential for proteolytic processing and cell entry of Marburg virus glycoprotein, unlike Ebola virus, and suggests Sec61 as a therapeutic target.

The paper compares MERS-CoV variants from Arabian and African camels, showing Arabian viruses are more resistant to inhibition by human soluble DPP4 due to the Q1020R mutation in the spike protein.

The paper characterizes the XEC SARS-CoV-2 lineage and evaluates the neutralization effect of JN.1 booster vaccination against KP.3.1.1 and XEC variants.

This study investigates the virological traits of the SARS-CoV-2 BA.2.87.1 lineage, finding it efficiently enters human cells but is more sensitive to antibody neutralization than JN.1.

This study identifies an ACE2-independent pathway for sarbecovirus entry in human cells, mediated by TMPRSS2-related proteases and linked to reduced antibody neutralization.

This study shows that defective interfering particles (DIPs) primarily exert antiviral activity through interferon (IFN) system activation rather than suppression of viral replication.

This study shows that the B.1.617.2 variant of SARS-CoV-2 evades antibodies from infection and vaccination, increases lung cell entry, and enhances cell fusion.

The paper shows that SARS-CoV-2 mutations from mink reduce antibody neutralization, suggesting potential risks for human infections.

This study shows camostat mesylate inhibits SARS-CoV-2 by blocking TMPRSS2 and its metabolite GBPA also has antiviral activity, suggesting no resistance through TMPRSS2-related proteases.

The paper shows that 2019-nCoV uses ACE2 and TMPRSS2 for cell entry, identifies TMPRSS2 as a therapeutic target, and demonstrates neutralization by SARS patient serum.