Lack of effect of mouse adenovirus type 1 infection on cell surface expression of major histocompatibility complex class I antigens.
It has been proposed that adenoviruses establish and maintain persistent infections by reducing the class I major histocompatibility complex-associated presentation of viral antigens to cytotoxic T lymphocytes, leading to ineffective cell-mediated immunity and impaired clearance of infected cells (W.S.M. Wold and L. R. Gooding, Virology 184:1-8, 1991). Early region 3 of human adenovirus types 2 and 5 encodes a 19-kDa glycoprotein that associates with the class I major histocompatibility complex (MHC) antigens in the endoplasmic reticulum and prevents their maturation and transport to the cell surface. Early region 1A of human adenovirus type 12 encodes a protein that inhibits class I MHC mRNA production at the transcriptional or posttranscriptional processing level. Unlike human adenovirus infections, however, mouse adenovirus type 1 (MAV-1) infection of a variety of cell types did not affect the surface expression of 10 different mouse class I MHC allotypes. MAV-1-infected cells also regenerated cell surface class I MHC antigens following proteolytic removal as efficiently as mock-infected cells. The ability of cells to present antigen to class I MHC (Kb)-ovalbumin-specific T-cell hybridoma cells was likewise unaltered by MAV-1 infection. Thus, the ability of MAV-1 to persist cannot be explained by the model of reduced class I MHC-associated antigen presentation proposed for human adenoviruses.
Kring
S C
SC
Department of Genetics, University of Georgia, Athens 30602-7223, USA.
Spindler
K R
KR
D000257:Adenoviridae Infections / Q000276:immunology*; D000260:Adenoviruses, Human / Q000276:immunology*; D000818:Animals; D017951:Antigen Presentation; D002460:Cell Line; D005434:Flow Cytometry; D015395:Histocompatibility Antigens Class I / Q000276:immunology*; D006801:Humans; D006825:Hybridomas; D051379:Mice; D013601:T-Lymphocytes / Q000276:immunology
D015395:Histocompatibility Antigens Class I