Murine cytomegalovirus interacts with major histocompatibility complex class I molecules to establish cellular infection.
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-2Dd and Kb molecules were most efficient. Monoclonal antibodies specific for the alpha 1 and/or alpha 2 domains of Dd and Kb 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 alpha 1 domain of Dd when in correct configuration with the alpha 2 and alpha 3 domains. In MCMV-resistant RMA-S cells, an improvement in the conformation of class I molecules introduced susceptibility to infection.
Wykes
M N
MN
Department of Microbiology, University of Western Australia, Nedlands.
Shellam
G R
GR
McCluskey
J
J
Kast
W M
WM
Dallas
P B
PB
Price
P
P
D000818:Animals; D003587:Cytomegalovirus / Q000254:growth & development*; D003586:Cytomegalovirus Infections / Q000382:microbiology*; D004252:DNA Mutational Analysis; D005805:Genes, MHC Class I; D015395:Histocompatibility Antigens Class I / Q000378:metabolism*; D007739:L Cells; D051379:Mice; D011487:Protein Conformation; D011991:Receptors, Virus / Q000378:metabolism*; D011994:Recombinant Proteins / Q000378:metabolism; D013329:Structure-Activity Relationship; D014162:Transfection
D015395:Histocompatibility Antigens Class I; D011991:Receptors, Virus; D011994:Recombinant Proteins