| Title: | A unique variant of lymphocytic choriomeningitis virus that induces pheromone binding protein MUP: Critical role for CTL |
| Author(s): | Ware BC; Sullivan BM; LaVergne S; Marro BS; Egashira T; Campbell KP; Elder J; Oldstone MBA; |
| Address: | "Viral-Immunobiology Laboratory, Department of Immunology and Microbiology, The Scripps Research Institute, La Jolla, CA 92037. Department of Molecular Physiology, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 52242. Department of Biophysics, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 52242. Department of Neurology, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 52242. Howard Hughes Medical Institute, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 52242. Department of Immunology and Microbiology, The Scripps Research Institute, La Jolla, CA 92037. Viral-Immunobiology Laboratory, Department of Immunology and Microbiology, The Scripps Research Institute, La Jolla, CA 92037; mbaobo@scripps.edu" |
| ISSN/ISBN: | 1091-6490 (Electronic) 0027-8424 (Print) 0027-8424 (Linking) |
| Abstract: | "Lymphocytic choriomeningitis virus (LCMV) WE variant 2.2 (v2.2) generated a high level of the major mouse urinary protein: MUP. Mice infected with LCMV WE v54, which differed from v2.2 by a single amino acid in the viral glycoprotein, failed to generate MUP above baseline levels found in uninfected controls. Variant 54 bound at 2.5 logs higher affinity to the LCMV receptor alpha-dystroglycan (alpha-DG) than v2.2 and entered alpha-DG-expressing but not alpha-DG-null cells. Variant 2.2 infected both alpha-DG-null or -expressing cells. Variant 54 infected more dendritic cells, generated a negligible CD8 T cell response, and caused a persistent infection, while v2.2 generated cytotoxic T lymphocytes (CTLs) and cleared virus within 10 days. By 20 days postinfection and through the 80-day observation period, significantly higher amounts of MUP were found in v2.2-infected mice. Production of MUP was dependent on virus-specific CTL as deletion of such cells aborted MUP production. Furthermore, MUP production was not elevated in v2.2 persistently infected mice unless virus was cleared following transfer of virus-specific CTL" |
| Keywords: | Animals CD8-Positive T-Lymphocytes/*immunology Dystroglycans/immunology Gene Expression Regulation/*immunology Lymphocytic Choriomeningitis/*immunology/pathology Lymphocytic choriomeningitis virus/*immunology Mice Proteins/*immunology Mup cytotoxic T lymp; |
| Notes: | "MedlineWare, Brian C Sullivan, Brian M LaVergne, Stephanie Marro, Brett S Egashira, Toru Campbell, Kevin P Elder, John Oldstone, Michael B A eng T32 AI007036/AI/NIAID NIH HHS/ HHMI/Howard Hughes Medical Institute/ U54 NS053672/NS/NINDS NIH HHS/ R21 AI145374/AI/NIAID NIH HHS/ R01 AI009484/AI/NIAID NIH HHS/ R01 AI099699/AI/NIAID NIH HHS/ Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't 2019/08/21 Proc Natl Acad Sci U S A. 2019 Sep 3; 116(36):18001-18008. doi: 10.1073/pnas.1907070116. Epub 2019 Aug 19" |
