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 persiste nt 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. Weld and L. R. Gooding, Virology 184:1-8, 1991). Early region 3 of human adenovirus types 2 and 5 encodes a 19-k Da glycoprotein that associates with the class I major histocompatibil ity complex (MHC) antigens in the endoplasmic reticulum and prevents t heir maturation and transport to the cell surface. Early region 1A of human adenovirus type 12 encodes a protein that inhibits class I MHC m RNA production at the transcriptional or posttranscriptional processin g level. Unlike human adenovirus infections, however, mouse adenovirus type 1 (MAV-1) infection of a variety of cell types did not affect th e surface expression of 10 different mouse class I MHC allotypes. MAV- 1-infected cells also regenerated cell surface class I MHC antigens fo llowing proteolytic removal as efficiently as mock-infected cells. The ability of cells to present antigen to class I MHC (K-b)-ovalbumin-sp ecific T-cell hybridoma cells was likewise unaltered by MAV-1 infectio n. Thus, the ability of MAV-1 to persist cannot be explained by the mo del of reduced class I MHC-associated antigen presentation proposed fo r human adenoviruses.