Complement receptor type 2 mediates infection of the human CD4-negative Raji B-cell line with opsonized HIV.
Opsonization of the HTLV-RF and HTLV-IIIB strains of HIV-1 with normal human HIV seronegative serum under conditions that allow complement activation resulted in the productive infection of cells of the Raji B lymphoblastoid cell line. Under the same experimental conditions, no infection of Raji cells was observed with unopsonized virus. Infection of Raji cells with complement-opsonized HIV-1 was totally suppressed by preblocking the function of CR2 (the C3dg receptor, CD21) on the cells with a monoclonal anti-CR2 antibody cross-linked with rabbit F(ab')2 anti-mouse immunoglobulin antibodies. Infection of Raji cells occurred independently of CD4 since the cells lacked the expression of CD4 antigen and of CD4 transcripts. Thus, Raji cells may be infected with complement-opsonized HIV independently of CD4 and in the absence of antibodies. By mediating and/or enhancing HIV infection, complement and complement receptors contribute to extend the range of target cells to the virus and may increase infection in patients with a low viral load.
D000163:Acquired Immunodeficiency Syndrome / Q000209:etiology*; D001402:B-Lymphocytes; D015152:Blotting, Northern; D002460:Cell Line; D003165:Complement System Proteins / Q000276:immunology*; D015497:HIV-1 / Q000472:pathogenicity*; D006801:Humans; D009895:Opsonin Proteins; D012194:RNA-Directed DNA Polymerase / Q000096:biosynthesis; D017464:Receptors, Complement 3d / Q000276:immunology*
D009895:Opsonin Proteins; D017464:Receptors, Complement 3d; D003165:Complement System Proteins; D012194:RNA-Directed DNA Polymerase