V3 Induces in Human Normal Cell Populations an Accelerated Macrophage-Mediated Proliferation- Apoptosis Phenomenon of Effector T Cells When They Respond to Their Cognate Antigen

Dys-Regulation of Effector CD4+ T Cell Function by the V3 Domain of the HIV-1 gp120 during Antigen Presentation

“…The result shows that in our model culture system the macrophages at the moment of their interaction with the memory T cells (CD4ϩ/ CD45ROϩ) can display on their surface structurally intact V3 lipopeptide. This result corroborates with our proposed model of costimulatory activity of the V3 region in the culture system during the antigen presentation process (3).…”

Simple Electrostatic Interaction Mechanisms in the Service of HIV‐1 Pathogenesis

“…1A). It has been demonstrated that the semiconserved principal neutralizing domain (PND) of V3 of the HIV-1 gp120 presented on the surface of monocyte-derived macrophages delivers a V3-specific signal of activation-apoptosis to CD45RO þ / CD4 þ T lymphocytes during the process of presentation of a recall antigen [13,14]. Recent evidence indicates that the recipient on the host membrane that interacts with V3 is the chemokine receptor CCR5 [13,15] (Fig.…”

Characterization of the interaction between peptides derived from the gp120/V3 domain of HIV-1 and the amino terminal of the chemokine receptor CCR5 by NMR spectroscopy and light scattering

“…Viral entry to a target cell is a complex process that involves three steps: (i) viral attachment mediated by the interaction of HIV-1 coat glycoprotein gp120 and target cell receptor CD4, (ii) gp120-co-receptor binding (CCR5 for infective HIV-1 R5 variants), and (iii) membrane fusion mediated by the viral glycoprotein gp41 [9]. A potential mechanism by which the virus appears during CCR5 binding to deregulate the physiological function of these cells at the immune synapse of antigen presentation has been identified, using synthetic peptides [10,11]. Ionic interactions between the variable V3 domain of the HIV-1 coat glycoprotein gp120 and the amino terminal of the chemokine receptor CCR5-Nt appear to play a prominent role in this process [12,13].…”