Julian D. J. Sng

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 shows glycaemic variability, not just hyperglycaemia, increases heart muscle dysfunction and myocardial injury risk in diabetes using genetic and experimental models.

This study shows that AVE0991, a Mas receptor agonist, reduces cytokines and viral titres in vitro but worsens disease in vivo in viral respiratory infections.

This study investigates how influenza A virus infection alters host cell glycosylation, identifying changes in sialic acid levels and glycan structures, and linking these to viral mechanisms and host responses.

This study compares SARS-CoV-2 Omicron variants' effects on nasal epithelial ciliated cells, finding increased tropism and dysfunction in BA.5 and XBB compared to BA.1 and ancestral virus.

This study shows SARS-CoV-2 infects hiPSC-derived neurons via endosomal-lysosomal pathway dependent on cathepsins, leading to HIF1alpha accumulation and phosphorylated tau, suggesting neurodegenerative effects.

The paper evaluates vaccine-induced and hybrid immunity against SARS-CoV-2 variants in two cohorts, finding reduced antibody titres and neutralization activity against Omicron variants, with some recovery after multiple vaccinations.

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 study shows that ZIKV envelope glycosylation mutants V153D and N154D, selected in Rag1-/- mice, replicate more efficiently in vitro and in organoids, suggesting N-linked glycosylation is not essential for envelope folding and trafficking.

This study shows that Down syndrome brain organoids with choroid plexus defects enhance SARS-CoV-2 neurotropism, which can be inhibited by targeting TMPRSS2 and Furin.

This study shows senolytic drugs reduce brain aging and COVID-19-related neuropathology by targeting senescent cells in human brain organoids and mice.

The paper shows Omicron SARS-CoV-2 lineages rely on ACE2 without TMPRSS2 complexes for entry, due to changes in the ACE2 Collectrin-Like Domain affecting TMPRSS2 activation.

The paper generates the first chromosome-length annotated genomes and transcriptomes of black and mute swans, revealing immune system limitations and plumage-related genetic differences.

This study shows SARS-CoV-2 activates microglial NLRP3 inflammasome via spike-ACE2 interaction, potentially linking viral infection to neurological symptoms like Parkinson's.