Differential HIV-1 endocytosis and susceptibility to virus infectio...
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):. doi: 10.1128/JVI.01051-12. Epub
2012 Jul 11.Differential HIV-1 endocytosis and susceptibility to virus infection in human macrophages correlate with cell activation status.1, , .1Centre de Recherche en Infectiologie, Centre Hospitalier Universitaire de Québec-CHUL, Canada.AbstractHIV-1 is an enveloped virus that enters target cells by fusion either directly at the plasma membrane or at the endosomal membrane. The latter mechanism follows a rapid engulfment of HIV-1 after its receptor engagement at the cell surface, and its scale depends on cellular endocytosis/degradation rates and virus fusion kinetics. HIV-1 has recently been shown to exploit a novel Pak1-dependent macropinocytosis mechanism as a way to productively infect macrophages. However, macrophages are highly heterogeneous cells that can adapt functionally to their changing environment, and their endosomal/lysosomal pathway is highly regulated upon cell activation. These changes might impact the ability of HIV-1 to exploit endocytosis as a way to productively infect macrophages. In this study, we compared HIV-1 endocytosis/degradation rates in nonactivated, M1-activated, and M2a-activated monocyte-derived macrophages (MDMs). We found that the rate of HIV-1 endocytosis was increased in M1-activated but decreased in M2a-activated MDMs. However, both M1 and M2a activations of MDMs led specifically to a greater clathrin-mediated endocytosis of HIV-1, which was independent of CD4 and CCR5 binding. Furthermore, clathrin-mediated endocytosis is unlikely to result in productive HIV-1 infection, given that it leads to increased viral degradation. Therefore, we suggest that viral fusion following endocytosis is restricted in activated macrophages.PMID:
[PubMed - indexed for MEDLINE] PMCID: PMC3457310 HIV-1 internalization is differentially modulated in M1- and M2a-activated MDMs. MDMs were first differentiated for 7 either left untreated (M0), treated with IFN-γ (20 ng/ml) and LPS (100 ng/ml) (M1), or treated with IL-4 (20 ng/ml) (M2a) for 18 h (top) or 72 h (bottom); and then allowed to internalize equal amounts of NL4-3Balenv virus (standardized in terms of p24) for 2.5 h at 37°C. After a 5-min trypsin treatment to remove membrane-bound viruses, cell lysis was performed. The total intracellular p24 content was quantified by an ELISA and normalized for cell viability (Cellular viability test see Materials and Methods). Results are expressed as fold changes compared to M0 and represent mean values (triplicate samples) of several independent experiments (*, P & 0.05; **, P & 0.01). In each graph, one symbol represents MDMs from one specific blood donor.J Virol. ):.Differences in viral degradation are not solely responsible for modulation of HIV-1 internalization in activated MDMs. MDMs were first differentiated for 7 either left untreated (M0), treated with IFN-γ (20 ng/ml) and LPS (100 ng/ml) (M1), or treated with IL-4 (20 ng/ml) (M2a) for 72 and then pretreated or not with bafilomycin A1 (final concentration of 100 nM) for 30 min. Cells were than allowed to internalize equal amounts of NL4-3Balenv virus (standardized in terms of p24), in the presence of the drug, for 2.5 h at 37°C. After a 5-min trypsin treatment to remove membrane-bound viruses, cell lysis was performed. The total intracellular p24 content was quantified by an ELISA and normalized for cell viability (Cellular viability test on uninfected cells). Results are expressed as fold changes compared to M0 for M1-activated (top) and M2a-activated (bottom) MDMs and represent mean values (triplicate samples) of several independent experiments. In each graph, one symbol represents MDMs from one specific blood donor.J Virol. ):.MDM activation acts on a CD4/CCR5-independent HIV-1 endocytosis pathway. MDMs were differentiated for 7 either left untreated (M0), treated with IFN-γ (20 ng/ml) and LPS (100 ng/ml) (M1), or treated with IL-4 (20 ng/ml) (M2a) for 72 and then allowed to internalize equal amounts of NL4-3env- (A), NL4-3env-/JRFLenv (B), or NL4-3env-/VSV-G (C) (standardized in terms of p24) for 2.5 h at 37°C. After a 5-min trypsin treatment to remove membrane-bound viruses, cell lysis was performed. The total intracellular p24 content was quantified by an ELISA and normalized for cell viability (Cellular viability test on uninfected cells). Results are expressed as fold changes compared to M0 and represent mean values (triplicate samples) of several independent experiments (*, P & 0.05; **, P & 0.01; ***, P & 0.001). Each symbol represents MDMs from one specific blood donor, and identical symbols are linked to the same donor in panels A to C.J Virol. ):.Macropinocytosis is not involved in HIV-1 endocytosis in both resting and activated MDMs. MDMs were differentiated for 7 either left untreated (M0), treated with IFN-γ (20 ng/ml) and LPS (100 ng/ml) (M1), or treated with IL-4 (20 ng/ml) (M2a) for 72 and then pretreated with EIPA or the equivalent amount of the drug vehicle alone (i.e., DMSO) for 30 min. Cells were then allowed to internalize equal amounts of NL4-3Balenv, NL4-3env-, NL4-3env-/VSV-G, or NL4-3env-/JRFLenv virus (standardized in terms of p24) for 2.5 h at 37°C. After a 5-min trypsin treatment to remove membrane-bound viruses, cell lysis was performed. The total intracellular p24 content was quantified by an ELISA and normalized for cell viability (Cellular viability test on uninfected drug-treated cells). Results are expressed as percentages of intracellular p24 levels compared to that of transporter-treated cells (100%) and represent mean values (triplicate samples) of several independent experiments. Each symbol represents MDMs from one specific blood donor, and identical symbols are linked to the same donor in the different panels.J Virol. ):.Clathrin-mediated endocytosis is involved in HIV-1 internalization in activated MDMs. MDMs were differentiated for 7 either left untreated (M0), treated with IFN-γ (20 ng/ml) and LPS (100 ng/ml) (M1), or treated with IL-4 (20 ng/ml) (M2a) for 72 and then pretreated with CPZ or the equivalent amount of the drug vehicle alone (i.e., ethanol) for 30 min. Cells were then allowed to internalize equal amounts of NL4-3Balenv, NL4-3env-, NL4-3env-VSV-G, or NL4-3env-/JRFLenv virus (standardized in terms of p24) for 2.5 h at 37°C. After a 5-min trypsin treatment to remove membrane-bound viruses, cell lysis was performed. The total intracellular p24 content was quantified by an ELISA and normalized for cell viability (Cellular viability test on uninfected cells). Results are expressed as percentages of the intracellular p24 level compared to that of transporter-treated cells (100%) and represent mean values (triplicate samples) of several independent experiments (*, P & 0.05; **, P & 0.01). Each symbol represents MDMs for one specific blood donor, and identical symbols are linked to the same donor in the different panels.J Virol. ):.HIV-1 replication is restricted in both classically and alternatively activated MDMs. MDMs were differentiated for 7 either left untreated (M0), treated with IFN-γ (20 ng/ml) and LPS (100 ng/ml) (M1), or treated with IL-4 (20 ng/ml) (M2a) for 72 and then put in contact with similar amounts of NL4-3Balenv (A) or NL4-3luc+env-R+/JRFLenv (B) virus (standardized in terms of p24) for 2 h at 37°C to allow virus infection. (A) Virus in the cell culture supernatant was quantified over time for 10 days by measuring the p24 content with an in-house ELISA. Results are expressed as the fold p24 production compared to that of M0-infected MDMs on day 3 and represent means ± standard errors of the means from 3 independent experiments. (B) Luciferase activity (expressed in relative light units [RLU]) was quantified on day 10 following virus infection, as described in Materials and Methods. Results are expressed as fold changes compared to values for M0-infected MDMs and represent means ± standard errors of the means from 5 independent experiments performed in triplicate (*, P & 0.05; **, P & 0.01; ****, P & 0.0001).J Virol. ):.HIV-1 degradation is increased in M1 and M2a MDMs. MDMs were differentiated for 7 either left untreated (M0), treated with IFN-γ (20 ng/ml) and LPS (100 ng/ml) (M1), or treated with IL-4 (20 ng/ml) (M2a) for 72 and then left untreated (A) or pretreated with bafilomycin A1 (100 nM) (B) for 30 min at 37°C before allowing them to internalize NL4-3Balenv or NL4-3env-/VSV-G virus for 2 h at 37°C. Cells were then washed, trypsinized to remove bound viruses (time zero), and incubated at 37°C (in the presence of the drug or not) to allow for virus degradation. The intracellular p24 content was quantified over time by an ELISA after cell lysis. Results are expressed as fold changes compared to the initial amount of intracellular p24 at time zero and represent means ± standard errors of the means from 5 (A) and 2 (B) independent experiments performed in triplicate (*, P & 0.05).J Virol. ):.Publication TypesMeSH TermsSubstancesGrant SupportFull Text SourcesOther Literature SourcesMedicalMiscellaneous
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出门在外也不愁Lineage-specific growth inhibition of NK cell lines by FOXO3 in ass...
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):.e6. doi: 10.1016/j.exphem.. Epub
2012 Aug 22.Lineage-specific growth inhibition of NK cell lines by FOXO3 in association with Akt activation status.1, , , , , , , , , , .1Division of Molecular Medicine, Aichi Cancer Center Research Institute, Nagoya, Japan.AbstractFOXO3 and PRDM1 are located on 6q21, one of the most frequently deleted regions among natural killer (NK) cell neoplasms. We previously demonstrated that forced expression of each gene suppresses the proliferation of NK cell lines with the 6q deletion. In this study, the forced expression of FOXO3 or PRDM1 was performed in various cell lines to clarify these suppressive effects. Forced expression of PRDM1 suppressed the proliferation of not only NK cell lines, but also other broad lineage cell lines. On the other hand, forced expression of FOXO3 was only effective on NK cell lines. FOXO3 functions as a transcriptional factor when it is localized in nuclei. Akt is known to induce cytoplasmic localization of FOXO3 as a result of phosphorylation. Transduced FOXO3 was predominantly localized in nuclei of NK cell lines, while it was localized in the cytoplasm of all non-NK cell lines. NK cell lines showed significantly lower Akt activity compared to other lineage cell lines. The low Akt activity and nucleic localization of FOXO3 in NK cell neoplasms seemed to cause NK cell-specific suppression. These findings indicate the "functional lineage specificity" of FOXO3 and the possibility for NK cell-specific gene therapy with minimal unexpected effects.Copyright (C) 2012 ISEH - Society for Hematology and Stem Cells. Published by Elsevier Inc. All rights reserved.PMID:
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