Human immunodeficiency virus and host cell lipids. Interesting pathways in research for a new HIV therapy

Raulin, J

doi:10.1016/s0163-7827(01)00019-4

Cited by 78 publications

(63 citation statements)

References 151 publications

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“…Interestingly, the Met 20 motif, which is required for Nef-associated block in MHC-I recycling from the ARF6 (small GTPase SDP ribosylation factor 6) compartment [18]. Interestingly, Nef can increase HIV infectivity by enhancing biosynthesis of lipid rafts as well as coupling newly synthesized cholesterol to lipid rafts and virus particles [19].…”

Section: Discussionmentioning

confidence: 99%

HIV‐1 down‐regulates the expression of CD1d via Nef

et al. 2006

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HIV‐1 has evolved several strategies to subvert host immune responses to the infected cells. One is to inhibit CTL recognition by HIV‐1 Nef‐mediated down‐regulation of MHC‐I expression on the surface of infected cells. Here we report that Nef also reduces the expression of the non‐classical MHC‐I like CD1d molecule, a third lineage of antigen‐presenting molecule, which presents lipid antigens. Nef achieves this by increasing internalization of CD1d molecules from the cell surface and retaining CD1d in the trans‐Golgi‐network (TGN). This effect depends on a tyrosine‐based motif present in CD1 cytoplasmic tail as well as the actions of four Nef motifs, which are known to be involved in the down‐regulation of MHC‐I or CD4. These results suggest that Nef regulates intracellular trafficking of CD1d via a distinct but shared pathway with MHC‐I and CD4. Thus, HIV‐1 reduces the visibility of its infected cells not only to MHC‐I‐restricted T cells but also to CD1d‐restricted NKT cells. Given that CD1d‐restricted T cells have unique effector and regulatory functions in innate and adapted immune responses as compared with their counterpart MHC‐restricted T cells, our data provide additional new insights into molecular basis of HIV‐1‐mediated damage to the immune system.

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Section: Discussionmentioning

confidence: 99%

HIV‐1 down‐regulates the expression of CD1d via Nef

et al. 2006

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“…[19][20][21][22][23][24][25][26] It has been recently demonstrated that CXCR4 requires an association with membrane lipid rafts for proper signaling function. 27,28 These membrane domains are rich in sphingolipids and cholesterol, which form a lateral assembly in a saturated glycerophospholipid environment. 29 The raft domains are known to serve as moving platforms on the cell surface, and are more ordered and resistant to nonionic detergents than are other areas of membranes.…”

Section: Introductionmentioning

confidence: 99%

Transplantation studies in C3-deficient animals reveal a novel role of the third complement component (C3) in engraftment of bone marrow cells

et al. 2004

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Mice deficient in complement C3 (C3 À/À ) are hematologically normal under steady-state conditions, and yet displayed a significant delay in hematopoietic recovery from either irradiation or transplantation of wild-type (WT) hematopoietic stem/ progenitor cells (HSPC). Transplantation of histocompatible WT Sca-1 þ cells into C3 À/À mice resulted in a (i) decrease in day 12 CFU-S, (ii) 5-7-day delay in platelet and leukocyte recovery, and (iii) reduced number of BM CFU-GM progenitors at day 16 after transplantation. Nevertheless, HSPC from C3 À/À mice engrafted normally into irradiated WT mice, suggesting that there was a defect in the hematopoietic environment of C3 À/À mice. Since C3 À/À mice cannot activate/cleave C3, the C3 fragments C3a, C3a des-Arg , and iC3b were examined for a role in HSPC engraftment. Liquid-phase C3a and C3a des-Arg increased CXCR4 incorporation into membrane lipid rafts (thus potentiating HSPC responses to SDF-1 gradients), whereas iC3b was deposited onto irradiated BM cells and functioned to tether CR3(CD11b/CD18) þ HSPC to damaged stroma. The activity of C3a des-Arg suggested that C3aR þ HSPC also expressed the C5L2 (receptor for C3a and C3a des-Arg ) and this was confirmed. In conclusion, a novel mechanism for HSC engraftment was identified, which involves complement activation and specific C3 fragments that promote conditioning for transplantation and enhance HSPC engraftment.

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“…Although retroviral gene products drive the replication cycle, recent studies have made it clear that host cell proteins and lipids play critical roles in many phases of this cycle. Lipid rafts in the membranes of infected T-cells have been shown to be essential for budding and entry of retroviruses such as human immunodeficiency virus (HIV) 1 and human T-cell lymphotrophic virus type 1 (1)(2)(3)(4)(5)(6). Lipid rafts are highly specialized regions of the plasma membrane characterized by a high content of cholesterol, sphingolipids, and glycosylphosphatidylinositol-anchored proteins (7).…”

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confidence: 99%