Infection of mesangial cells with HIV and SIV: Identification of GPR1 as a coreceptor

Tokizawa, Shigemi; Shimizu, Nobuaki; Liu, Huiyu; Fang, Deyu; Haraguchi, Yuji; Oite, Takashi; Hoshino, Hiroo

doi:10.1046/j.1523-1755.2000.00207.x

Cited by 38 publications

(21 citation statements)

References 46 publications

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“…In 1992, Green et al [53] first showed that cultured renal mesangial cells could be infected by HIV-1. These findings were confirmed and expanded 8 years later by Tokizawa et al [54], who identified the chemokine receptor GPR1 as playing a critical role in this process, and by Conaldi et al [55], who found that the establishment of a persistent infection in these cells stimulates the synthesis of cytokines that could lead to glomerulosclerosis. In contrast, to date other investigators have been unable to infect cultured mesangial cells [56,57], and HIV-1 transcripts have not been found in mesangial cells from patients with HIVAN [58].…”

Section: Mesangial Hyperplasiamentioning

confidence: 68%

A 20-year history of childhood HIV-associated nephropathy

Ray

Rakusan

et al. 2004

Pediatr Nephrol

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In 1984, physicians in New York and Miami reported HIV-infected adult patients with heavy proteinuria and rapid progression to end-stage renal disease. These patients showed large edematous kidneys with a combination of focal segmental glomerulosclerosis (FSGS) and tubulointerstitial lesions. This renal syndrome, named HIV-associated nephropathy (HIVAN), was found predominantly in African Americans. Subsequent studies confirmed the presence of HIVAN in children, who frequently develop nephrotic syndrome in association with FSGS and/or mesangial hyperplasia with microcystic tubular dilatation. Since then, substantial progress has been made in our understanding of the etiology and pathogenesis of HIVAN. This article reviews 20 years of research into the pathogenesis of HIVAN and discusses how these concepts could be applied to the treatment of children with HIVAN. HIV-1 infection plays a direct role in the pathogenesis of childhood HIVAN, at least partially by affecting the growth and differentiation of glomerular and tubular epithelial cells and enhancing the renal recruitment of infiltrating mononuclear cells and cytokines. An up-regulation of renal heparan sulfate proteoglycans seems to play a relevant role in this process, by increasing the recruitment of heparin-binding growth factors (i.e., FGF-2), chemokines, HIV-infected cells, and viral proteins (i.e., gp120, Tat). These changes enhance the infectivity of HIV-1 in the kidney and induce injury and proliferation of intrinsic renal cells. Highly active anti-retroviral therapy (HAART) appears to be the most promising treatment to prevent the progression of childhood HIVAN. Hopefully, in the near future, better education, prevention, and treatment programs will lead to the eradication of this fatal childhood disease.

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Section: Mesangial Hyperplasiamentioning

confidence: 68%

A 20-year history of childhood HIV-associated nephropathy

Ray

Rakusan

et al. 2004

Pediatr Nephrol

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“…This observation raised the possibility that CCR2 might be involved in selective viral amplification in mucosal lymphocytes, the predominant site of replication during acute infection, but our results suggest that is not the case. In contrast, GPR1, GPR15, and APJ are not known to be expressed on CD4 ϩ T lymphocytes, although GPR1 is expressed on and reportedly supports in vitro HIV-1 infection of several nonlymphoid target cells (51,54). Within the genital tract, CCR2 and CCR3 are expressed in both female and male genital mucosa (36,41) although little is known about mucosal tissue expression of the other GPCRs used by HIV-1.…”

Section: Discussionmentioning

confidence: 99%

Heterosexual Transmission of Human Immunodeficiency Virus Type 1 Subtype C: Macrophage Tropism, Alternative Coreceptor Use, and the Molecular Anatomy of CCR5 Utilization

Isaacman-Beck

Hermann

et al. 2009

J Virol

104

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Human immunodeficiency virus type 1 transmission selects for virus variants with genetic characteristics distinct from those of donor quasispecies, but the biological factors favoring their transmission or establishment in new hosts are poorly understood. We compared primary target cell tropisms and entry coreceptor utilizations of donor and recipient subtype C Envs obtained near the time of acute infection from Zambian heterosexual transmission pairs. Both donor and recipient Envs demonstrated only modest macrophage tropism, and there was no overall difference between groups in macrophage or CD4 T-cell infection efficiency. Several individual pairs showed donor/recipient differences in primary cell infection, but these were not consistent between pairs. Envs had surprisingly broad uses of GPR15, CXCR6, and APJ, but little or no use of CCR2b, CCR3, CCR8, GPR1, and CXCR4. Donors overall used GPR15 better than did recipients. However, while several individual pairs showed donor/recipient differences for GPR15 and/or other coreceptors, the direction of the differences was inconsistent, and several pairs had unique alternative coreceptor patterns that were conserved across the transmission barrier. CCR5/CCR2b chimeras revealed that recipients as a group were more sensitive than were donors to replacement of the CCR5 extracellular loops with corresponding regions of CCR2b, but significant differences in this direction were not consistent within pairs. These data show that sexual transmission does not select for enhanced macrophage tropism, nor for preferential use of any alternative coreceptor. Recipient Envs are somewhat more constrained than are donors in flexibility of CCR5 use, but this pattern is not universal for all pairs, indicating that it is not an absolute requirement.A majority of new human immunodeficiency virus type 1 (HIV-1) infections are initiated by only a single genetic species, although in some, several closely related variants are transmitted (19,26,34,44,55). Nevertheless, in all cases, a molecular bottleneck occurs during transmission (8,15,22,33,56). This bottleneck does not appear to be simply a stochastic result of low-efficiency transmission since viral sequences in recipients do not typically reflect the majority sequences in donors, even in genital secretions responsible for transmission (22,56). Identifying the biological factors that favor particular variants in transmission and/or establishment in new hosts is essential both to understanding the mechanisms of transmission and to developing approaches, including vaccines and microbicides, that might interrupt transmission.More than 15 years ago, it was recognized that new infections were nearly always initiated by HIV-1 variants that were macrophage tropic and non-syncytium inducing (NSI) in T-cell lines, even though donors often harbored variants that were syncytium inducing (SI) and non-macrophage tropic (55). The molecular basis for these characteristics was subsequently linked to use of the entry coreceptor CCR5 by macrophagetropic/...

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“…The etiology of HIV nephropathy is unclear, but there is evidence that direct infection of renal tubular and/or mesangial cells by HIV-1 may be a significant factor (18). It is also unclear why this disease afflicts principally African American men, but it is now the third most common etiology of endstage renal disease among African Americans aged 20 -64 years after diabetes and hypertension (17,19).…”

Section: Demand For Kidney Transplantationmentioning

confidence: 99%

Evolving Clinical Strategies for Transplantation in the HIV-Positive Recipient

Stock

Roland

2007

Transplantation

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The transplant community has been slow to recognize the efficacy of highly active antiretroviral therapy in changing the course of human immunodeficiency virus (HIV) infection to a chronic condition. People infected with HIV are dying less often from progression of HIV to acquired immune deficiency syndrome. Unfortunately, there is an increasing rate of morbidity and mortality from comorbidities resulting in end-stage liver and kidney disease, prompting some transplant centers to eliminate HIV infection as a contraindication to transplantation. This overview will describe the evolving clinical strategies that have resulted in good outcomes after solid organ transplantation in the HIV-positive recipient.

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Infection of mesangial cells with HIV and SIV: Identification of GPR1 as a coreceptor

Cited by 38 publications

References 46 publications

A 20-year history of childhood HIV-associated nephropathy

A 20-year history of childhood HIV-associated nephropathy

Heterosexual Transmission of Human Immunodeficiency Virus Type 1 Subtype C: Macrophage Tropism, Alternative Coreceptor Use, and the Molecular Anatomy of CCR5 Utilization

Evolving Clinical Strategies for Transplantation in the HIV-Positive Recipient

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