Mechanisms of opsonized HIV entry in normal B lymphocytes

FEBS Letters

Legendre, Christophe¹  Dormont, Dominique¹  Richard, Yolande²  Galanaud, Pierre²  Krzysiek, Roman²  Gras, Gabriel¹ 

[1] Service de Neurovirologie, CE-FAR, DSV/DRM/SNV, IPSC, 60-68 avenue de la Division Leclerc, BP 6, 92265 Fontenay aux Roses Cédex, France;INSERM U131, IPSC, 32 rue des carnets, 92140 Clamart, France

关键词: B lymphocyte;    CD4;    Complement receptor;    CD21;    CD35;    HIV;    C′-ADE;    complement-antibody-dependent enhancement;    CR;    complement receptor;    EBV;    Epstein-Barr virus;    GC;    germinal center;    HIV;    human immunodeficiency virus;    IL;    interleukin;    mAb;    monoclonal antibody;    SCR;    short consensus repeat;   

DOI  :  10.1016/0014-5793(96)00040-3

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Using our in vitro model of normal B cell infection that functions with low doses of HIV but requires virus opsonization by seropositive patient serum, and complement, we analyzed what receptors allowed virus entry. Here, we show that HIV infection of B cells occurs through 2 major receptors: the CD4 antigen and the CR1/CR2 complex. These 2 pathways work independently since a complete inhibition of virus entry requires both CD4 and CD21/CD35 blockade on CD4^dim tonsillar B cells whereas only the latter is critical on CD4-negative B cells.

【 授权许可】

Unknown