Envelope glycoproteins from biologically diverse isolates of immunodeficiency viruses have widely different affinities for CD4.

Ivey-Hoyle, Mona; Culp, Jeffrey S.; Chaikin, Margery A.; Hellmig, Brian D.; Matthews, Thomas J.; Sweet, Raymond W.; Rosenberg, Martin

doi:10.1073/pnas.88.2.512

Cited by 122 publications

(93 citation statements)

References 25 publications

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“…The role of entry is favoured by genetic studies in which the determinants of tropism map to the env region Liu et al, 1990;O'Brien et al, 1990;Chesebro et al, 1991;Hwang et al, 1991 ;Shioda et al, 1991 ;Westervelt et al, 1991), although alterations in the structure of the envelope glycoproteins might conceivably influence the assembly of virions at late stages of replication. The precise stage at which tropism is determined is undefined but generally perceived to be a post-binding event, given that all isolates have in common a high affinity for CD4 (Brighty et al, 1991;Ivey-Hoyle et al, 1991;Moore et al, 1992). Fusion of the viral and cellular membranes is a candidate step, although a recent study using fluorescence dequenching suggests that tropism is determined by a post-fusion event (Potash et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

Definition of the range and distribution of human immunodeficiency virus macrophage tropism using PCR-based infectivity measurements

Collin

Illei

James

et al. 1994

Journal of General Virology

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The tropism of human immunodeficiency virus (HIV) for macrophages (m~b) is a well recognized phenomenon, but the range and distribution of m~b-tropic phenotypes have not been defined by quantitative means. This study uses a PCR-based infectivity assay to derive an index of m~ tropism for several common strains of HIV. The results show that m~b tropism varies over about six orders of magnitude and that the most m~b-tropic strains have a higher infectivity for m~b than for peripheral blood lymphocytes. Strains were distributed throughout this range, suggesting that m~b tropism is a continuously variable phenotypic property. Although the degree of tropism was strongly influenced by the mode of isolation and propagation of virus strains, there was no evidence for the existence of distinct m~b-tropic or non-m~b-tropic phenotypes. Finally, the tropism of two selected strains was found to be determined by an early step in replication, probably virus entry.

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Section: Discussionmentioning

confidence: 99%

Definition of the range and distribution of human immunodeficiency virus macrophage tropism using PCR-based infectivity measurements

Collin

Illei

James

et al. 1994

Journal of General Virology

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“…Anti-CD3 (IgG2a-clone ϫ 35; Immunotech-Coulter), anti-CD28 (IgG1; Becton Dickinson), and isotype-matched irrelevant mAbs (Becton Dickinson) as well as full-length synthetic HIV-1 Tat protein (86 aa, derived from the HIV-1 T cell line-tropic BH10 strain; Technogen, Caserta, Italy) (27) were resuspended in PBS containing 0.1% BSA (Sigma, St. Louis, MO). Forty-eight-well flat-bottom polystyrene plates (Costar, Cambridge, MA) were coated overnight at 4°C with anti-CD3, anti-CD28, isotype-matched irrelevant mAb (IgG1 and IgG2a; Immunotech-Coulter), Tat, BSA, used alone or in combination, at the concentrations indicated in the text.…”

Section: Adherence Of Abs and Proteins To Microtiter Platesmentioning

confidence: 99%

Engagement of CD28 Modulates CXC Chemokine Receptor 4 Surface Expression in Both Resting and CD3-Stimulated CD4+ T Cells

Secchiero

Zella

Curreli

et al. 2000

The Journal of Immunology

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Optimal CD4+ T cell activation requires the cooperation of multiple signaling pathways coupled to the TCR-CD3 complex and to the CD28 costimulatory molecule. In this study, we have investigated the expression of surface CXC chemokine receptor 4 (CXCR4) in enriched populations of CD4+ T PBL, stimulated with anti-CD3 and anti-CD28 mAbs, immobilized on plastic. Anti-CD3 alone induced a progressive down-regulation of surface CXCR4, accompanied by a significant decline in the entry of the HXB2 T cell line-tropic (X4-tropic) HIV-1 clone in CD4+ T cells. Of note, this effect was strictly dependent on the presence in culture of CD14+ monocytes. On the other hand, anti-CD28 alone induced a small but reproducible increase in the expression of surface CXCR4 as well as in the entry of HXB2 HIV-1 clone in resting CD4+ T cells. When the two mAbs were used in combination, anti-CD28 potently synergized with anti-CD3 in inducing the expression of CD69 activation marker and stimulating the proliferation of CD4+ T cells. On the other hand, anti-CD28 counteracted the CXCR4 down-modulation induced by anti-CD3. The latter effect was particularly evident when anti-CD28 was associated to suboptimal concentrations of anti-CD3. Because CXCR4 is the major coreceptor for the highly cytopathic X4-tropic HIV-1 strains, which preferentially replicate in proliferating CD4+ T cells, the ability of anti-CD28 to up-regulate the surface expression of CXCR4 in both resting and activated CD4+ T cells provides one relevant mechanism for the progression of HIV-1 disease.

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“…These include adenovirusbased expression of gp120, yielding 2-5 mg from 10 6 infected cells (Natuk et al 1992) and constitutive expression at about 1 mg per mL of culture medium from transformed CHO cells (Laskey et al 1986). In addition, regulated expression in a Drosophila cell line allowed gp120 production, usually at a level of 2 mg/mL and, though probably much less often, at 30 mg/mL (Ivey-Hoyle et al 1991) at a cell density of 10 7 cells/mL. However, the products are likely to be less authentic than those produced in mammalian cells because of differences in glycosylation and other metabolic pathways between insect and mammalian cells.…”

Section: Introductionmentioning

confidence: 99%

Sendai virus‐based expression of HIV‐1 gp120: reinforcement by the V(−) version

Yu¹,

Shioda²,

Kato³

et al. 1997

Genes to Cells

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Background: We have established a system for recovering Sendai virus (SeV), a nonsegmented negative strand RNA virus, entirely from cDNA at an extremely high rate, and have succeeded in creating a V(-) SeV whose gene expression was greatly enhanced by the deletion of the nonessential V gene. Because of its extreme medical importance, there has been a strong need for the establishment of a better system to express the gp120 envelope glycoprotein of the human immunodeficiency virus type 1 (HIV-1) in sufficient quantity and purity. It also remains to be established to produce gp120 in in vitro natural host cells for HIV-1 such as human primary blood mononuclear cells, macrophages or established T cell lines.

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Envelope glycoproteins from biologically diverse isolates of immunodeficiency viruses have widely different affinities for CD4.

Abstract: The envelope glycoprotein gp120 of primate immunodeficiency viruses initiates viral attachment to CD4' cells by binding to the CD4 antigen on host cell surfaces.

Cited by 122 publications

References 25 publications

Definition of the range and distribution of human immunodeficiency virus macrophage tropism using PCR-based infectivity measurements

Definition of the range and distribution of human immunodeficiency virus macrophage tropism using PCR-based infectivity measurements

Engagement of CD28 Modulates CXC Chemokine Receptor 4 Surface Expression in Both Resting and CD3-Stimulated CD4+ T Cells

Sendai virus‐based expression of HIV‐1 gp120: reinforcement by the V(−) version

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