Introduction

The growth cycles and oncogenic properties of the murine and human retroviruses are inextricably linked to the immune system. Those viruses that cause leukaemias, lymphomas or immunodeficiencies do so by infecting and often activating immune cells. Conversely, those retroviruses that induce solid tumours must evolve ways to aid the host cell in evading the cellular immune system. One major molecular mechanism by which these retroviruses can either activate or evade the immune system is by control of MHC class I antigen expression in the cells they infect. An effect of murine retrovirus infection on MHC antigen expression was first suspected in the late 1970s, when it was observed that thymocytes obtained from animals several weeks after infection with leukaemia viruses appeared to express higher levels of MHC class I antigens than thymic cells from control animals. Conversely, down-regulation of MHC expression on solid tumours induced by oncogene-containing (sarcoma) retroviruses had also been observed. Because of the experimental constraints of these in vivo systems, however, proof of a causal relationship between retrovirus infection and MHC regulation was lacking. More recent studies have demonstrated a direct action of retroviruses on MHC gene regulation and have begun to elucidate the ways in which these compact viruses, with only 6000–10 000 bases of coding sequence, regulate the histocompatibility antigen expression of their host cells.

Murine leukaemia virusesy

The murine retroviruses can be broadly divided into two classes: the leukaemia viruses and the sarcoma viruses.