Area of research
Infectious Diseases · Immunology
Research interest
Research interests include SARS-CoV-2 and COVID-19 Research, interferon and immune responses, Viral gastroenteritis research and epidemiology, and COVID-19 Clinical Research Studies.
The population context is a driver of the heterogeneous response of epithelial cells to interferons
Transcriptomics-inferred dynamics of SARS-CoV-2 interactions with host epithelial cells
Extended methods for spatial cell classification with DBSCAN-CellX
Influence of cell type specific infectivity and tissue composition on SARS-CoV-2 infection dynamics within human airway epithelium
Genetic regulation of OAS1 nonsense-mediated decay underlies association with COVID-19 hospitalization in patients of European and African ancestries
A diabetic milieu increases ACE2 expression and cellular susceptibility to SARS-CoV-2 infections in human kidney organoids and patient cells
A family of conserved bacterial virulence factors dampens interferon responses by blocking calcium signaling
The FDA-Approved Drug Cobicistat Synergizes with Remdesivir To Inhibit SARS-CoV-2 Replication <i>In Vitro</i> and Decreases Viral Titers and Disease Progression in Syrian Hamsters
Type III and Not Type I Interferons Efficiently Prevent the Spread of Rotavirus in Human Intestinal Epithelial Cells
Increased Sensitivity of SARS-CoV-2 to Type III Interferon in Human Intestinal Epithelial Cells
USP22 controls type III interferon signaling and SARS-CoV-2 infection through activation of STING
A model for network-based identification and pharmacological targeting of aberrant, replication-permissive transcriptional programs induced by viral infection
USP22 controls type III interferon signaling and SARS-CoV-2 infection through activation of STING
Protocol for SARS-CoV-2 infection of kidney organoids derived from human pluripotent stem cells
A Model for Network-Based Identification and Pharmacological Targeting of Aberrant, Replication-Permissive Transcriptional Programs Induced by Viral Infection
TMPRSS2 expression dictates the entry route used by SARS‐CoV‐2 to infect host cells
Single‐cell analyses reveal SARS‐CoV‐2 interference with intrinsic immune response in the human gut
Single‐cell transcriptomics reveals immune response of intestinal cell types to viral infection
SARS‐CoV‐2 infection remodels the host protein thermal stability landscape
Functional comparison of MERS-coronavirus lineages reveals increased replicative fitness of the recombinant lineage 5
Genetic regulation of <i>OAS1</i> nonsense-mediated decay underlies association with risk of severe COVID-19
Conserved Induction of Distinct Antiviral Signalling Kinetics by Primate Interferon Lambda 4 Proteins
The endogenous cellular protease inhibitor SPINT2 controls SARS-CoV-2 viral infection and is associated to disease severity
Adapting Gastrointestinal Organoids for Pathogen Infection and Single Cell Sequencing under Biosafety Level 3 (BSL-3) Conditions
Dynamics of SARS-CoV-2 host cell interactions inferred from transcriptome analyses
A diabetic <i>milieu</i> increases cellular susceptibility to SARS-CoV-2 infections in engineered human kidney organoids and diabetic patients
Increased sensitivity of SARS-CoV-2 to type III interferon in human intestinal epithelial cells
Network-based identification and pharmacological targeting of host cell master regulators induced by SARS-CoV-2 infection
Conserved induction of distinct antiviral signalling kinetics by primate interferon lambda 4 proteins
Adapting Gastrointestinal Organoids for Pathogen Infection and Single Cell Sequencing under Biosafety Level 3 (BSL-3) Conditions