The expression of stable, correctly folded major histocompatibility complex class I molecules conferred susceptibility to murine cytomegalovirus (MCMV) in cells which were previously resistant to infection, demonstrating that these molecules interact critically with MCMV to initiate infection. All class I molecules could potentiate MCMV infection but H-2D(d) and K(b) molecules were most efficient. Monoclonal antibodies specific for the alpha1 and/or alpha2 domains of D(d) and K(b) inhibited infection. Infection of L cells transfected with hybrid major histocompatibility complex class I molecules demonstrated that allelic control of susceptibility to MCMV mapped to the alpha1 domain of D(d) when in correct configuration with the alpha2 and alpha3 domains. In MCMV-resistant RMA-S cells, an improvement in the conformation of class I molecules introduced susceptibility to infection.
|Journal||Journal of Virology|
|Publication status||Published - 1993|