This study assessed the impact of various donor variables on isolation outcomes (yield and viability) and posttransplant engraftment, using the SCID/Alb-uPA (severe combined immunodeficient/urokinase type plasminogen activator under the control of an albumin promoter) human liver chimeric mouse model.
To investigate whether immune components can influence the kinetics of virion decay, we analyzed viral dynamics in immunodeficienturokinase-type plasminogen activator chimera mice.
Expanding on our demonstration that acylated peptides derived from the large HBV envelope protein block virus entry in vitro, we show their applicability to prevent HBV or woolly monkey hepatitis B virus infection in vivo, using immunodeficienturokinase-type plasminogen activator (uPA) mice repopulated with primary human or Tupaia belangeri hepatocytes.
Human hepatocytes were transplanted into urokinase-type plasminogen activator-transgenic SCID mice (uPA/SCID mice), which are immunodeficient and undergo liver failure.
Here, we report partial repopulation of the liver of immunodeficienturokinase-type plasminogen activator (uPA)/recombinant activation gene-2 (RAG-2) mice with normal human hepatocytes isolated from the adult liver.