Seema S. Lakdawala

This study analyzes an H5N5 influenza virus isolate that caused a human fatality, finding it lacks key traits associated with human pandemic potential.

The paper identifies a disrupted CCR5-like immunoglobulin gene in black-footed ferrets linked to increased susceptibility to plague caused by Yersinia pestis.

The paper assesses transmission efficiency of D1.1 H5N1 strains in ferrets, finding only one human isolate efficiently transmits, linked to the PB2 D701N mutation.

The study assesses the pandemic risk of a fatal zoonotic H3N8 influenza virus from chickens, finding it has moderate pandemic potential due to its ability to infect humans and replicate in human cells.

The paper develops chicken lung organoids to model avian influenza virus-host interactions and finds they contain diverse cell types and express relevant viral infection genes.

This study examines within-host evolutionary dynamics of influenza A virus in humans and ferrets, finding that genetic drift limits selection efficiency in humans but not in ferrets.

This study identifies innate antiviral readiness as a key driver of TSCM cell expansion, showing its predictive value for viral clearance and vaccine design.

The paper investigates H5N1 transmission on dairy farms by sampling air, wastewater, and milk, finding infectious virus in air and wastewater, viral RNA in cow breath, and subclinical infections in cows.

This study shows that pre-existing H1N1 immunity protects ferrets from severe disease caused by bovine H5N1 influenza virus.

This study shows that ventilation rates do not affect influenza virus transmission efficiency in a ferret playpen setup with close-range interactions and fomites.

The paper assesses the pandemic risk of swine H1N2 influenza viruses by analyzing their transmission potential and immune response in ferrets.

This study shows that influenza-infected macrophages release viral ribonucleoproteins (vRNPs) that trigger inflammatory responses in uninfected cells through the RIG-I/MDA5 pathway.

The paper uses fluorescence in situ hybridization and point process models to infer the sequence of vRNP associations during influenza A virus assembly.