bioluminescent imaging reveals divergent viral pathogenesis in two strains of stat1-deficient mice, and in α？γ interferon receptor-deficient mice生物荧光成像揭示了不同病毒的发病机理两株stat1-deficient老鼠,在α缺少γ干扰素受体的老鼠们注入了.pdf

Bioluminescent Imaging Reveals Divergent Viral Pathogenesis in Two Strains of Stat1-Deficient Mice, and in aßc Interferon Receptor-Deficient Mice 1 2 3 3 3 Tracy Jo Pasieka , Lynne Collins , Megan A. O’Connor , Yufei Chen , Zachary M. Parker , Brent L. 3 2 3 Berwin , David R. Piwnica-Worms , David A. Leib * 1 Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St Louis, Missouri, United States of America, 2 BRIGHT Institute, Molecular Imaging Center, Mallinckrodt Institute of Radiology, Washington University School of Medicine, St Louis, Missouri, United States of America, 3 Department of Microbiology and Immunology, Dartmouth Medical School, Lebanon, New Hampshire, United States of America Abstract Pivotal components of the IFN response to virus infection include the IFN receptors (IFNR), and the downstream factor signal transducer and activator of transcription 1 (Stat1). Mice deficient for Stat1 and IFNR (Stat12/ 2 and IFNaßcR2/ 2 mice) lack responsiveness to IFN and exhibit high sensitivity to various pathogens. Here we examined herpes simplex virus type 1 (HSV-1) pathogenesis in Stat12/ 2 mice and in IFNaßcR2/ 2 mice following corneal infection and bioluminescent imaging. Two divergent and paradoxical patterns of infection were observed. Mice with an N-terminal deletion in Stat1 (129Stat1 2/ 2 (N-term)) had transient infection of the liver and spleen, but succumbed to encephalitis by day 10 post-infection. In stark contrast, infection of IFNaßcR2/ 2 mice was rapidly fatal, with associated viremia and fulminant infection of the liver and spleen, with infected infiltrating cells being primarily of the monoc