Apoptosis induced in synchronized human immunodeficiency virus type 1-infected primary peripheral blood mononuclear cells is detected after the peak of CD4+ T-lymphocyte loss and is dependent on the tropism of the gp120 envelope glycoprotein

Lawson, Victoria; Silburn, Katherine A.; Gorry, Paul R; Paukovic, Geza; Purcell, Damian F. J.; Greenway, Alison L.; McPhee, Dale A.

doi:10.1016/j.virol.2004.06.012

Cited by 10 publications

(10 citation statements)

References 74 publications

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“…Levels of secreted p24 antigen increased earlier and reached a higher plateau following infection with treated virus (Fig 2E), similar to results seen with X4 NL-EGFP infection. As reported by other investigators (Blanco et al, 2001, Grivel et al, 2000, Lawson et al, 2004), infection with the R5-tropic clone of JR-CSF resulted in less cell death than infection with the X4-tropic clone of NL4-3. The JR-CSF infected cell cultures were maintained for 14 days, at which point cells with integrated HIV DNA and replication competent virus (infectious units per million cells, IUPM) were assayed.…”

Section: Resultssupporting

confidence: 79%

CD44 MicroBeads accelerate HIV-1 infection in T cells

2009

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Super-paramagnetic CD44 MicroBeads (Miltenyi) designed for the isolation of infectious HIV-1 from dilute or difficult biological samples dramatically enhance the infectivity of bound HIV virions, even if the original viral suspension is merely incubated with beads. Infection of the CEM T cell line with the NL4-3 virus clone or primary human CD4 T cells with X4- and R5-tropic clones and a clade C primary virus isolate all showed accelerated p24 production and larger fractions of infected target cells. Effects could be detected very early; incubation of virus with the CD44 MicroBeads promoted higher levels of viral integration within the first infection cycle. In summary, CD44 MicroBeads provide the means not only to concentrate dilute viral samples, but also to directly facilitate within days rather than weeks the in vitro expansion of patient isolates independent of coreceptor usage and the performance of HIV replication assays that require a large fraction of infected primary T cells.

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Section: Resultssupporting

confidence: 79%

CD44 MicroBeads accelerate HIV-1 infection in T cells

2009

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“…The fact that gag/pro and env gene expression dramatically increased vector-induced apoptosis in our study is a novel finding that should be considered in strategies to modify the immunogenicity of poxvirus-based vectors. Perhaps this effect should not be surprising, because numerous studies have documented the proapoptotic effects of HIV gp120 (2,3,27,30,32,41). The effects of expression of the Gag protein on apoptosis are less certain, but we have observed apoptotic nuclear changes in mammalian cells upon expression of the Gag protein (unpublished observations).…”

Section: Discussionmentioning

confidence: 59%

Direct Comparison of Antigen Production and Induction of Apoptosis by Canarypox Virus- and Modified Vaccinia Virus Ankara-Human Immunodeficiency Virus Vaccine Vectors

Zhang

Cassis-Ghavami

Eller³

et al. 2007

J Virol

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Recombinant poxvirus vectors are undergoing intensive evaluation as vaccine candidates for a variety of infectious pathogens. Avipoxviruses, such as canarypox virus, are replication deficient in mammalian cells by virtue of a poorly understood species-specific restriction. Highly attenuated vaccinia virus strains such as modified vaccinia virus Ankara (MVA) are similarly unable to complete replication in most mammalian cells but have an abortive-late phenotype, in that the block to replication occurs post-virus-specific DNA replication. In this study, an identical expression cassette for human immunodeficiency virus gag, pro, and env coding sequences was placed in canarypox virus and MVA vector backbones in order to directly compare vector-borne expression and to analyze differences in vector-host cell interactions. Antigen production by recombinant MVA was shown to be greater than that from recombinant canarypox virus in the mammalian cell lines and in the primary human cells tested. This observation was primarily due to a longer duration of antigen production in recombinant MVA-infected cells. Apoptosis induction was found to be more profound with the empty canarypox virus vector than with MVA. Remarkably, however, the inclusion of a gag/pro/env expression cassette altered the kinetics of apoptosis induction in recombinant MVA-infected cells to levels equal to those found in canarypox virus-infected cells. Antigen production by MVA was noted to be greater in human dendritic cells and resulted in enhanced T-cell stimulation in an in vitro antigen presentation assay. These results reveal differences in poxvirus vector-host cell interactions that should be relevant to their use as immunization vehicles.

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“…Apoptosis induction is a major pathway in HIV pathogenesis [Levy, 2009]. In addition to HIV infection and gp120 Lawson et al, 2004], even Tat is involved in the modulation of cell proliferation and survival by induction of cellular pro-apoptotic or anti-apoptotic responses that vary depending on the cell type and Tat concentration Milani et al, 1998;Barillari and Ensoli, 2002]. Tat can promote cell survival and proliferation in some cell lineages at picomolar/nanomolar concentrations, whereas, at higher concentrations (nanomolar/ micromolar), Tat induces apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Analysis of the effects of HIV‐1 Tat on the survival and differentiation of vessel wall‐derived mesenchymal stem cells

Gibellini

Miserocchi

Tazzari³

et al. 2012

J of Cellular Biochemistry

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HIV infection is an independent risk factor for atherosclerosis development and cardiovascular damage. As vessel wall mesenchymal stem cells (MSCs) are involved in the regulation of vessel structure homeostasis, we investigated the role of Tat, a key factor in HIV replication and pathogenesis, in MSC survival and differentiation. The survival of subconfluent MSCs was impaired when Tat was added at high concentrations (200-1,000 ng/ml), whereas lower Tat concentrations (1-100 ng/ml) did not promote apoptosis. Tat enhanced the differentiation of MSC toward adipogenesis by the transcription and activity upregulation of PPARγ. This Tat-related modulation of adipogenesis was tackled by treatment with antagonists of Tat-specific receptors such as SU5416 and RGD Fc. In contrast, Tat inhibited the differentiation of MSCs to endothelial cells by downregulating the expression of VEGF-induced endothelial markers such as Flt-1, KDR, and vWF. The treatment of MSCs with Tat-derived peptides corresponding to the cysteine-rich, basic, and RGD domains indicated that these Tat regions are involved in the inhibition of endothelial marker expression. The Tat-related impairment of MSC survival and differentiation might play an important role in vessel damage and formation of the atherosclerotic lesions observed in HIV-infected patients.

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Apoptosis induced in synchronized human immunodeficiency virus type 1-infected primary peripheral blood mononuclear cells is detected after the peak of CD4+ T-lymphocyte loss and is dependent on the tropism of the gp120 envelope glycoprotein

Cited by 10 publications

References 74 publications

CD44 MicroBeads accelerate HIV-1 infection in T cells

CD44 MicroBeads accelerate HIV-1 infection in T cells

Direct Comparison of Antigen Production and Induction of Apoptosis by Canarypox Virus- and Modified Vaccinia Virus Ankara-Human Immunodeficiency Virus Vaccine Vectors

Analysis of the effects of HIV‐1 Tat on the survival and differentiation of vessel wall‐derived mesenchymal stem cells

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