An Anthropoid-Specific Locus of Orphan C to U RNA-Editing Enzymes on Chromosome 22

Jarmuz, Adam; Chester, Ann; Bayliss, Jayne; Gisbourne, Jane; Dunham, Ian; Scott, James; Navaratnam, Naveenan

doi:10.1006/geno.2002.6718

Cited by 633 publications

(730 citation statements)

References 34 publications

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“…A3G is found in human T lymphocytes, monocytes, and macrophages, and lethally hypermutates viral DNA shortly after it is synthesized by RT (11)(12)(13)(14)(15). A3G was also demonstrated in testes, ovaries, and a number of tumor cell lines (14).…”

Section: Stimulation Of Cell Surface Ccr5 and Cd40 Molecules By Theirmentioning

confidence: 99%

Stimulation of Cell Surface CCR5 and CD40 Molecules by Their Ligands or by HSP70 Up-Regulates APOBEC3G Expression in CD4+ T Cells and Dendritic Cells

Pido-Lopez

Whittall

Wang

et al. 2007

The Journal of Immunology

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Apolipoprotein B mRNA-editing, enzyme-catalytic, polypeptide-like-3G (A3G) is an intracellular innate antiviral factor that deaminates retroviral cytidine to uridine. In an attempt to harness the anti-HIV effect of A3G, we searched for an agent that would up-regulate A3G and identify the receptors involved. Stimulation of cell surface CCR5 with CCL3 and CD40 with CD40L or both molecules with microbial 70-kDa heat shock protein (HSP)70 up-regulated A3G mRNA and protein expression in human CD4+ T cells and monocyte-derived dendritic cells (DC), demonstrated by real-time PCR and Western blots, respectively. The specificity of CCR5 and CD40 stimulation was established by inhibition with TAK 779 and mAb to CD40, as well as using human embryonic kidney 293 cells transfected with CCR5 and CD40, respectively. A dose-dependent increase of A3G in CCL3- or HSP70-stimulated CD4+ T cells was associated with inhibition in HIV-1 infectivity. To differentiate between the inhibitory effect of HSP70-induced CCR5 binding and that of A3G, GFP-labeled pseudovirions were used to infect human embryonic kidney 293 cells, which showed inhibition of pseudovirion uptake, consistent with A3G being responsible for the inhibitory effect. Ligation of cell surface CCR5 receptors by CCL3 or CD40 by CD40L activated the ERK1/2 and p38 MAPK signaling pathways that induced A3G mRNA expression and production of the A3G protein. These in vitro results were corroborated by in vivo studies in rhesus macaques in which A3G was significantly up-regulated following immunization with SIVgp120 and p27 linked to HSP70. This novel preventive approach may in addition to adaptive immunity use the intracellular innate antiviral effect of A3G.

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Section: Stimulation Of Cell Surface Ccr5 and Cd40 Molecules By Theirmentioning

confidence: 99%

Stimulation of Cell Surface CCR5 and CD40 Molecules by Their Ligands or by HSP70 Up-Regulates APOBEC3G Expression in CD4+ T Cells and Dendritic Cells

Pido-Lopez

Whittall

Wang

et al. 2007

The Journal of Immunology

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“…APOBEC3F (hA3F) and APOBEC3G (hA3G) are members of a family of related cytidine deaminases shown to have antiretroviral activity in vitro (1,8,9,11,14,23,29). In the absence of the human immunodeficiency virus type 1 (HIV-1) accessory protein Vif, hA3F and hA3G are incorporated into virions and induce G-to-A hypermutations in the viral genome (1,8,12,14,27,29,30).…”

mentioning

confidence: 99%

“…Further studies to elucidate the clinical utility of hA3G and hA3F may include the examination of CD4 ϩ T cells rather than PBMCs and follow a larger cohort over time to examine the predictive relationship on progression to AIDS. APOBEC3B (hA3B), another member of the APOBEC3 gene cluster on chromosome 22 (9), may also have anti-HIV effects (5,21), and this target may be evaluated in future studies. We also thank the staff of the St. Louis ACTU for their help in recruiting patients, Laura Blair for her dedicated technical assistance, and Diana Nurutdinova and Lisa Mahnke for their helpful discussions.…”

mentioning

confidence: 99%

APOBEC3F and APOBEC3G mRNA Levels Do Not Correlate with Human Immunodeficiency Virus Type 1 Plasma Viremia or CD4 ⁺ T-Cell Count

Cho¹,

Drechsler

Burke

et al. 2006

J Virol

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APOBEC3F and APOBEC3G (hA3F and hA3G) are part of an innate mechanism of antiretroviral defense. The human immunodeficiency virus type 1 (HIV-1) accessory protein Vif targets both proteins for proteasomal degradation. Using mRNA from peripheral blood mononuclear cells of 92 HIV-infected subjects not taking antiretroviral therapy and 19 HIV-uninfected controls, we found that hA3F (P < 0.001) and hA3G (P ‫؍‬ 0.016) mRNA levels were lower in HIV-infected subjects and were positively correlated with one another (P ‫؍‬ 0.003). However, we found no correlation in the abundance of either hA3F or hA3G mRNA with either viral load or CD4 counts in HIV-infected subjects.

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“…Vif-deficient virions produced from 'permissive' cells can infect 'nonpermissive' cells, but the virus subsequently produced is not infectious. The molecular nature of permissivity and the exact function of Vif in infection of nonpermissive cells was not known until recently when a series of reports showed that a host cellular protein known as APOBEC3G (apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3G) is a potent inhibitor of HIV infection in the nonpermissive cells [70,71]. APOBEC3G is a member of the cytidine deaminase family, which prevents viral cDNA synthesis via deaminating deoxycytidines (dC) in the minus-strand retroviral cDNA replication intermediate [72][73][74][75][76].…”

Section: Virus Infectivity Factor (Vif)mentioning

confidence: 99%

Roles of HIV-1 auxiliary proteins in viral pathogenesis and host-pathogen interactions

Pauza

et al. 2005

Cell Res

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Active host-pathogen interactions take place during infection of human immunodeficiency virus type 1 (HIV-1). Outcomes of these interactions determine the efficiency of viral infection and subsequent disease progression. HIVinfected cells respond to viral invasion with various defensive strategies such as innate, cellular and humoral immune antiviral mechanisms. On the other hand, the virus has also developed various offensive tactics to suppress these host cellular responses. Among many of the viral offensive strategies, HIV-1 viral auxiliary proteins (Tat, Rev, Nef, Vif, Vpr and Vpu) play important roles in the host-pathogen interaction and thus have significant impacts on the outcome of HIV infection. One of the best examples is the interaction of Vif with a host cytidine deaminase APOBEC3G. Although specific roles of other auxiliary proteins are not as well described as Vif-APOBEC3G interaction, it is the goal of this brief review to summarize some of the preliminary findings with the hope to stimulate further discussion and investigation in this exhilarating area of research.

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An Anthropoid-Specific Locus of Orphan C to U RNA-Editing Enzymes on Chromosome 22

Cited by 633 publications

References 34 publications

Stimulation of Cell Surface CCR5 and CD40 Molecules by Their Ligands or by HSP70 Up-Regulates APOBEC3G Expression in CD4+ T Cells and Dendritic Cells

Stimulation of Cell Surface CCR5 and CD40 Molecules by Their Ligands or by HSP70 Up-Regulates APOBEC3G Expression in CD4+ T Cells and Dendritic Cells

APOBEC3F and APOBEC3G mRNA Levels Do Not Correlate with Human Immunodeficiency Virus Type 1 Plasma Viremia or CD4 ⁺ T-Cell Count

Roles of HIV-1 auxiliary proteins in viral pathogenesis and host-pathogen interactions

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An Anthropoid-Specific Locus of Orphan C to U RNA-Editing Enzymes on Chromosome 22

Cited by 633 publications

References 34 publications

Stimulation of Cell Surface CCR5 and CD40 Molecules by Their Ligands or by HSP70 Up-Regulates APOBEC3G Expression in CD4+ T Cells and Dendritic Cells

Stimulation of Cell Surface CCR5 and CD40 Molecules by Their Ligands or by HSP70 Up-Regulates APOBEC3G Expression in CD4+ T Cells and Dendritic Cells

APOBEC3F and APOBEC3G mRNA Levels Do Not Correlate with Human Immunodeficiency Virus Type 1 Plasma Viremia or CD4 + T-Cell Count

Roles of HIV-1 auxiliary proteins in viral pathogenesis and host-pathogen interactions

Contact Info

Product

Resources

About

APOBEC3F and APOBEC3G mRNA Levels Do Not Correlate with Human Immunodeficiency Virus Type 1 Plasma Viremia or CD4 ⁺ T-Cell Count