Epstein-Barr virus uses HLA class II as a cofactor for infection of B lymphocytes

Quan Li(University of Missouri–Kansas City), Melanie K. Spriggs(University of Missouri–Kansas City), Susan Kovats(University of Missouri–Kansas City), Susan M. Turk(University of Missouri–Kansas City), Michael R. Comeau(University of Missouri–Kansas City), Barbara S. Nepom(University of Missouri–Kansas City), Lindsey Hutt‐Fletcher(University of Missouri–Kansas City)
Journal of Virology
June 1, 1997
Cited by 310Open Access
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Abstract

Infection of B lymphocytes by Epstein-Barr virus (EBV) requires attachment of virus via binding of viral glycoprotein gp350 to CD21 on the cell surface. Penetration of the cell membrane additionally involves a complex of three glycoproteins, gH, gL, and gp42. Glycoprotein gp42 binds to HLA-DR. Interference with this interaction with a soluble form of gp42, with a monoclonal antibody (MAb) to gp42, or with a MAb to HLA-DR inhibited virus infection. It was not possible to superinfect cells that failed to express HLA-DR unless expression was restored by transfection or creation of hybrid cell lines with complementing deficiencies in expression of HLA class II. HLA class II molecules thus serve as cofactors for infection of human B cells.


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