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J Gen Virol 75 (1994), 2755-2759; DOI 10.1099/0022-1317-75-10-2755
© 1994 Society for General Microbiology

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Replication of human cytomegalovirus in cells deficient in beta2-microglobulin gene expression

Q. H. Wu1, W. Trymbulak2, R. J. Tatake2, S. J. Forman3, R. A. Zeff2 and J. D. Shanley1

1 Department of Medicine
and2 Department of Pathology, University of Connecticut Health Center, Farmington, Connecticut
and3 Department of Hematology and Bone Marrow Transplantation, City of Hope National Medical Center, Duarte, California, U.S.A.

To study the roles of beta2-microglobulin (beta2-m) and major histocompatibility complex (MHC) class I expression in human cytomegalovirus (HCMV) infection, the ability of HCMV strain AD-169 to infect and replicate in a human melanoma cell line (FO-1), which is beta2-m-deficient and cannot express MHC class I on its cell surface, was examined. Susceptibility of FO-1 cells was compared with human foreskin fibroblasts (HFF) and FO-1H cells (FO-1 cells that have been transfected with the human beta2-m gene, restoring MHC I expression on the cell surface). As judged by the HCMV immediate early 1 (IE-1) antigen expression, HCMV was able to infect FO-1 cells, although somewhat less efficiently than HFF. However, the expression of HCMV late (L) antigen and the production of virus was significantly less for FO-1 cells than for HFF. Analysis of the FO-1H transfectants revealed that expression of IE-1 and L HCMV antigens was comparable to FO-1 cells, which lack MHC I. Treatment of FO-1 and FO-1H cells with sodium butyrate prior to inoculation did not alter the expression of MHC I in either cell type, but did increase susceptibility of both cell types to HCMV infection, as well as the expression of L antigens and production of virus. These studies indicate that HCMV infection of FO-1 cells is independent of beta2-m and MHC class I expression.

Received 27 January 1994; accepted 7 June 1994.





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Copyright © 1994 by the Society for General Microbiology.