Alexander A. Khromykh

This study uses human cerebral organoids to identify PHGDH as a key metabolic factor enabling WNV infection and a potential drug target.

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.

The paper optimizes reverse genetics methods for positive-sense RNA viruses, showing improved recovery efficiency using specific promoters and ribozymes.

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.

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 paper develops a bispecific antibody that targets both Nipah virus surface glycoproteins, reducing viral escape and enhancing protection against NiV disease.

This study identifies the PAZ domain's role in ensuring accurate 21 nt vsiRNA production by Dcr2 in Aedes aegypti, critical for antiviral responses against Semliki Forest virus.

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.

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

The paper uses long-read sequencing to investigate SARS-CoV-2 integration into the human genome and finds no evidence of such integration in infected cells.

The paper describes the development of a high-affinity Nanobody against SARS-CoV-2 RBD that neutralizes wild-type and D614G variants with nanomolar potency.