Introduction

Human adenoviruses (Ads) possess two well-studied mechanisms for modulation of MHC class I expression. The mechanism that is predominant in infected cells involves down-regulation of surface class I antigens caused by a block in the transport of class I heavy chains to the cell surface. This block is effected by a protein product of a viral early gene (termed E3) and seems to operate in cells infected with most virus serotypes. In adenovirus-transformed cells, the level of surface class I antigens can be either elevated or decreased depending on the serotype of the transforming adenovirus and is controlled mainly at the step of transcription of class I genes. Modulation of the rate of initiation of class I gene transcription in these cells is mediated by the product(s) of a different viral early gene (E1A). Interestingly, it is the expression of the E1A gene of highly oncogenic adenoviruses (such as Adl2) that results in down-regulation of class I transcription, providing a possible mechanism whereby oncogenic Adl2-transformed cells can escape host immune surveillance and form tumours. Adenovirus-infected and adenovirus-transformed cells are, therefore, interesting experimental systems for the study of class I modulation.

Adenovirus transformation and oncogenicity have been extensively reviewed (Knippers & Levine, 1989; Boulanger & Blair, 1991; Chinnadurai, 1992; Moran, 1993) and comprehensive reviews on virus structure, biology and pathogenicity are also available (Ginsberg, 1984; Doerfler, 1986; Horwitz, 1990a,b). The wider aspects of the immunobiology of adenoviruses have also been described (Wold & Gooding, 1991; Braithwaite et al, 1993).