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This article explores the cultural issues affecting the rural entrepreneur in Ghana. It is based upon the results of an enterprise development needs assessment tour conducted by the authors in Ghana for the Food and Agriculture Organisation, the objective of which was to assess the cultural factors which must be accounted for in the implementation of subsequent projects in the region.

SUMMARYIn vitro studies shows that recombinant tumour necrosis factor (TNF) α and β, and interferon-gamma (IFN-γ) can enhance HIV replication, and peripheral blood mononuclear cells (PBMC) infected with HIV in vitro secrete high levels of the same cytokines. As T cells secrete all three mediators, the capacity of T cell activation signals to trigger cytokine production in PBMC from HIV-infected individuals was investigated as such patients may be immunocompromised. We demonstrate that asymptomatic seropositives in CDC group II/III as well as patients who have progressed to CDC group IV of the disease proliferate efficiently to anti-CD3 antibody, recombinant interleukin-2 (rIL-2), phytohaemagglutinin (PHA), PHA plus phorbol 12, 13 dibutyrate (PMA) but secrete significantly (P>0.05) higher amounts of TNF-α, TNF-β and IFN-γ compared with controls in response to the same stimulants. We also show a difference between group II/III and group IV patients with the latter secreting more TNF-α and IFN-γ. The kinetics of TNF-α and -β and IFN-γ production was stimulus dependent with overall levels varying in time for each stimulus. Furthermore, the kinetics of the response to all three stimulants were altered in seropositives; CDC group II/III and group IV patients secreted higher levels of cytokines over several time points compared to controls. The altered production of these mediators by HIV-infected patients may contribute to disease progression and to the pathogenesis of AIDS.

Understanding why human immunodeficiency virus (HIV) preferentially infects some CD4(+) CD45RO(+) memory T cells has implications for antiviral immunity and pathogenesis. We report that differential expression of a novel secreted factor, ps20, previously implicated in tissue remodeling, may underlie why some CD4 T cells are preferentially targeted. We show that (i) there is a significant positive correlation between endogenous ps20 mRNA in diverse CD4 T-cell populations and in vitro infection, (ii) a ps20(+) permissive cell can be made less permissive by antibody blockade- or small-interference RNA-mediated knockdown of endogenous ps20, and (iii) conversely, a ps20(low) cell can be more permissive by adding ps20 exogenously or engineering stable ps20 expression by retroviral transduction. ps20 expression is normally detectable in CD4 T cells after in vitro activation and interleukin-2 expansion, and such oligoclonal populations comprise ps20(positive) and ps20(low/negative) isogenic clones at an early differentiation stage (CD45RO(+)/CD25(+)/CD28(+)/CD57(-)). This pattern is altered in chronic HIV infection, where ex vivo CD4(+) CD45RO(+) T cells express elevated ps20. ps20 promoted HIV entry via fusion and augmented CD54 integrin expression; both of these effects were reversed by anti-ps20 antibody. We therefore propose ps20 to be a novel signature of HIV-permissive CD4 T cells that promotes infection in an autocrine and paracrine manner and that HIV has coopted a fundamental role of ps20 in promoting cell adhesion for its benefit. Disrupting the ps20 pathway may therefore provide a novel anti-HIV strategy.

The use of PPD (purified protein derivative of tuberculin) as a carrier has several significant advantages. It provides very powerful T cell help and it gives rise to virtually no antibody response against itself. This is particularly useful if it is intended to go on to make monoclonal antibodies, where the presence of a large amount of anti-carrier antibody is a nuisance! Furthermore, unlike most comparably powerful adjuvant systems, it can be used in man. PPD coupling has been used to raise antibodies to haptens and to raise T cell responses to tumour cells. It is here reported that small peptides coupled to PPD will give rise to good titres of anti-peptide antibody. For peptides that contain no cysteine, coupling has been achieved by attaching succinimidyl 4-(N-maleimidomethyl) cyclohexane-1-carboxylate (SMCC) to the alpha-amino group of the peptide and N-succinimidyl 3-(2-pyridyldithio) propionate (SPDP) to the PPD and allowing an uncleavable bond to form between them. Data on immunization with the leucotactic nonapeptide of the alpha chain of the complement component C3 and with some oncogene-related peptides have been obtained.

A programmable and biodegradable drug delivery device is desirable when a drug needs to be administered locally. While most local drug delivery devices made of biodegradable polymers relied on the degradation of the polymers, the degradation-based release control is often limited by the property of the polymers. Thus, we propose micro-geometry as an alternative measure of controlling drug release. The proposed devices consist of three functional layers: diffusion control layer via micro-orifices, diffusion layer, and drug reservoir layers. A micro-fabrication technology was used to shape an array of micro-orifices and micro-cavities in 85/15PLGA layers. A thin layer of fast degrading 50/50PLGA was placed as the diffusion layer between the 85/15PLGA layers to prevent any burst-type release. To modulate the release of the devices, the dimension and location of the micro-orifices were varied and the responding in vitro release response of tetracycline was monitored over 2 weeks. The release response to the different micro-geometry was prominent and further analyzed by FEM simulation. Comparison of the experiments to the simulated results identified that the variation of micro-geometry influenced also the volume-dependent degradation rate and induced the osmotic pressure.

It is increasingly important to control cell growth into and within artificial scaffolds. Tissues such as skin, blood vessels, and cartilage have multi-layer structures with different cells in each layer. With the aid of micro-fabrication technology, a novel scaffolding method for biodegradable polymers such as polylactic acid (PLA), polyglycolic acid (PGA), and the copolymers poly(lactide-co-glycolide)(PLGA), was developed to construct three-dimensional multi-layer micro-fluidic tissue scaffolds. The method emphasizes micro-fluidic interconnections between layers within the scaffolds and maintenance of high-resolution geometries during the bonding process for the creation of multi-layered scaffolds. Micro-holes (10-100 microm), micro-channels, and micro-cavities were all created by micro-molding. Solvent-vapor based bonding of micro-molded layers preserved 20 microm sized structures. Sample scaffolds were constructed for purposes such as channel-directed cell growth and size-based cell sorting. Further extension of these techniques to create a micro-vascular network within or between layers is possible. Culturing of human coronary artery endothelial cells (HCAECs) on the sample scaffolds demonstrated the biocompatibility of the developed process and the strong influence of high-resolution micro-geometries on HCAEC growth.

The cellular basis of HIV associated dementia has been correlated with microglial activation and neuronal dysfunction in symptomatic HIV-1 disease. As a cellular model of HIV-1 infection of brain tissue in vitro, we established a stationary human brain aggregate (SHBA) system to compare infection of HIV-1 SF162 (R5 virus) to that of IIIB (X4 virus). Aggregates were analysed by immunohistochemistry, morphometry, flow cytometry and p24 ELISA. SHBAs had a 1 mm(3) size with a mixed cellular composition of 36% neurones, 27% astrocytes, 2% macrophages/microglia and 14% oligodendrocytes. Infection of SHBA's with the R5 HIV-1 SF162 virus led to the expression of HIV-1 p24 antigen in 6% of cells. Infection with this R5 using virus culminated in transient neuronal damage and a decrease in mitotically active progenitor cells within aggregates. Infection with X4 using HIV-1 IIIB was associated with astrocytosis and neurotoxicity. We propose that: (1) the pattern of cellular damage elicited by HIV-1 infection of brain tissue in vitro depends on virus subtype as determined by its preferential use of R5 or X4 chemokine receptors for entry into cells; (2) SHBAs are a reliable and readily established model of the cellular complexity of human brain tissue in vitro.

AIM To characterize HIV-1 Gag p24-specific CD4 cell responses in HIV-exposed-seronegative (ES) individuals. METHODOLOGY Twelve ES individuals, of diverse ethnicity and wild type for the CCR5 Delta-32 mutation, were identified. Controls were HIV-negative blood donors. Gag p24-specific and total Vbeta+ CD4 cells that expressed MIP-1beta, IFN-gamma and IL-2 were enumerated by intracytoplasmic cytokine staining. beta-Chemokine expression was correlated with susceptibility to R5 HIV-1 infection, as measured by polymerase chain reaction for integrated HIV-1 and by p24 enzyme-linked immunosorbent assay. RESULTS Similar numbers of mitogen-stimulated and Vbeta+ MIP-1beta+, IFN-gamma+ and IL-2+ T cells were found in ES and HIV-negative control subjects. However, all ES subjects tested had an HIV Gag p24-specific MIP-1beta+, IFN-gamma+ and IL-2+ CD4 T-cell response that was rare in controls. p24-Specific cells of all ES but no control subjects could be expanded by in-vitro Ag/IL-2 stimulation, and when re-stimulated with an overlapping peptide series showed evidence of a broad CD4 cell memory response directed against multiple regions of Gag p24. Mitogen-stimulated ES CD4 cells were as susceptible to HIV infection as those from control subjects, but p24-specific IFN-gamma+ CD4 cells of six out of seven ES subjects tested were less susceptible to R5 HIV-1 infection than the counterpart fraction depleted of p24-specific IFN-gamma+ cells. The addition of blocking anti-beta-chemokine antibodies did not promote R5 HIV-1 infection of p24-specific IFN-gamma+ cells. CONCLUSION Specific CD4 cell immunity, characterized by a broadly directed memory Gag-p24 CD4 cell response and reduced susceptibility of specific CD4 cells to R5 HIV-1 infection, is a likely correlate of non-transmission.

Two poly(L-lactide-co-epsilon-caprolactone) random copolymers containing 5 and 40 mol % of epsilon-CL, namely P(LA-co-CL(5)) and P(LA-co-CL(40)), respectively, have been made macroporous by freeze-drying solutions in dimethylcarbonate. Most of the freeze-dried foams, prepared by varying polymer concentration and cooling rate, exhibited two main pore populations: (1). longitudinally oriented tube-like macropores with diametersor=100 microm, and (2). interconnected micropores (10-100 microm). Pore characteristics, including macropore density, mean diameter, and interdistance, as well as micropore density, area, and shape, were determined by image analysis of scanning electron micrographs in order to study the influence of processing and formulation parameters on foam structure and properties. The pore orientation and the 3-D texture also were studied by image analysis and impedance spectroscopy. In the case of the P(LA-co-CL(5)), the macropore diameter increased with the cooling rate while the micropore diameter decreased. The micropores also became more circular when the cooling rate was increased. The pore size and morphology of the P(LA-co-CL(40)) were quite unchanged by varying the cooling rate. All the other conditions being the same, the P(LA-co-CL(5)) foams were better organized than the P(LA-co-CL(40)) foams, and pore orientation was improved at the higher cooling rate. Pore size and morphology also can be controlled by changing the polymer concentration (Cp), as we showed by studying P(LA-co-CL(5)) foams prepared by freeze-drying solutions in the 1-10 w/v % Cp range. Macropore density, average diameter, and interdistance of P(LA-co-CL(5)) foams increased with Cp, but the micropore characteristics remained almost unchanged no matter the Cp. The reliability of the characterization methods has been discussed, with special attention to mercury intrusion porosimetry, which is used primarily for measurement of pore volume and pore size distribution. However, this technique is reported here as a destructive and unreliable method for the characterization of fragile P(LA-co-CL(40)) foams. This study shows that image analysis and impedance spectroscopy can give reliable information relative to the pore morphology and anisotropy of freeze-dried foams.

Small and medium-size companies are increasingly competing globally by forming horizontal alliances. To support this process there is a growing need for formation of virtual teams across company boundaries that can jointly develop new products and processes. A review of previous research shows that, although virtual teams have been well defined as a concept, the key variables involved in the formation of inter-organisational teams and the managerial implications remain comparatively unknown. The chapter provides a process perspective for researching virtual team formation and interaction patterns. By combining cross-disciplinary theoretical approaches, the reported study offers a conceptual overview for collective teaming in virtual settings. The research findings so far confirm that virtual team formation and evolution follow specific development patterns, which can be described as cyclical self-energising processes.

BACKGROUND: HIV-1 strains R5 and X4 can infect CD4 memory T cells in vivo. Anti-CD3/28 stimulation induces beta-chemokines and CCR5 down-regulation and renders these cells resistant to R5 HIV-1 infection. Here we describe an additional cellular mechanism that blocks productive R5 HIV-1 infection of CD4 memory T cells. METHODS: Blood-derived CD4 memory T cells and CD4 T-cell clones were infected with primary R5 and X4 HIV-1 strains. Virus replication was correlated with CCR5 expression and beta-chemokine production. Virus entry and infectivity were measured by PCR for early and late products of HIV reverse transcription respectively. RESULTS: R5 strains were up to 1000-fold less infectious than X4 viruses for CD4 memory T cells. This resistance was independent of CCR5 levels and of the Delta-32 mutation and the CCR2-V64I/CCR5-59653T linked mutations. Blocking endogenous beta-chemokines relieved minimally this restriction. At the single cell level, CD4 memory cells were either permissive or non-permissive for R5 HIV-1 infection. R5 HIV titre was up to 10-fold lower than X4 virus titre even in a permissive clone. However, R5 viruses replicated as efficiently as X4 viruses in the permissive clone when neutralizing anti-beta chemokine antibodies were added. Non-permissive cells blocked a post-entry step of the virus life-cycle and expressed early but not late HIV transcripts. Neutralizing anti-beta chemokine antibodies promoted R5 virus replication marginally in the non-permissive clone. CONCLUSION: Some blood memory CD4 T cells retard R5 HIV-1 replication via endogenous beta-chemokines whereas others block productive R5 HIV-1 infection by an additional mechanism that interferes with a post-entry step of the virus life cycle. These natural barriers might contribute to lower pathogenicity of R5 HIV-1 strains for CD4 memory T cells than X4 viruses that emerge late in disease.

Enrichment of a subset of CD4(+)CD45R0(+)CD7(-) T cells has been observed in HIV-infected individuals. We have investigated the ability of CD7(+) and CD7(-) T cells to support replication of HIV and show that virus replicates preferentially in CD7(+) cells. Several possible mechanisms that may underlie such differences in susceptibility to HIV were studied. Our data demonstrate that mitogen stimulation induces poor expression of CD25 and IL-2 in CD7(-) compared with CD7(+) cells. We also show that uninfected CD7(-) cells are more resistant to mitogen-induced apoptosis than CD7(+) cells. Our data support the view that the CD7(-) subset is inherently resistant to HIV replication and that this is due in part to reduced CD25 expression and IL-2 production.

Enrichment of a subset of CD4(+)CD45R0(+)CD7(-) T cells has been observed in HIV-infected individuals. We have investigated the ability of CD7(+) and CD7(-) T cells to support replication of HIV and show that virus replicates preferentially in CD7(+) cells. Several possible mechanisms that may underlie such differences in susceptibility to HIV were studied. Our data demonstrate that mitogen stimulation induces poor expression of CD25 and IL-2 in CD7(-) compared with CD7(+) cells. We also show that uninfected CD7(-) cells are more resistant to mitogen-induced apoptosis than CD7(+) cells. Our data support the view that the CD7(-) subset is inherently resistant to HIV replication and that this is due in part to reduced CD25 expression and IL-2 production.

Publisher Summary This chapter describes a novel process to manufacture aligned discontinuous fiber composites using electric fields. It is demonstrated that the orientation of dielectric fibers like glass fibers (with and without polymer powder coating) can be effectively controlled using electric fields. Aligned discontinuous fiber composite (ADF) processes composites made of glass fibers and nylon-12 matrix provides significant improvements in stiffness and strength with fiber alignment. The effect of the microstructure on the performance of ADF composites has been established. Recent advances in the area of powder coating of fibers at MSU in combination with the phenomenon of aligning fibers in electric fields, has paved the way to conceptualize and develop the novel high-speed processing methodology that can manufacture aligned discontinuous fiber composites. Full realization of the stiffness to weight benefits of these composites is possible due to effective fiber alignment combined with the ability to pack and process at higher volume fraction of fibers. Absence of solvents or liquids in the ADF process improves the speed of processing many folds and makes the process environmental friendly. The fiber alignment technique of the ADF process is simple in operation and design, with the scope for retrofitting this technique in an existing composite sheet or lamination processing unit. Aligned discontinuous fiber composites are flexible and can be molded or stamped into complex parts. It is envisaged that ADF composites, with unique performance and processability capabilities, can expand the range of the applicability of discontinuous fiber thermoplastic composite materials to many areas in the automotive, infrastructure, and durable goods sectors.

Inter-organisational teams organised to explore a business opportunity are a relatively new area of research. The paper presents a conceptual overview for collective teaming in virtual settings. The findings of the study confirm that high performing teams follow special development patterns, which can be described as cyclical self-energising processes.

Using both conventional and laser confocal fluorescence microscopy, the intracellular distribution of galectin-1 in HeLa cells was analyzed and compared with the localization of previously documented markers of the nucleus and cytoplasm. The Sm epitopes of the small nuclear ribonucleoprotein complexes (snRNPs) and the non-snRNP splicing factor SC35 yielded only nuclear staining. On the other hand, the enzyme lactate dehydrogenase was cytoplasmic. In contrast to these patterns in which nuclear versus cytoplasmic localizations appeared to be mutually exclusive, galectin-1, as well as galectin-3, yielded simultaneous nuclear and cytoplasmic staining. Confocal microscopy showed galectin-1 fluorescence throughout most of the sections from the top of the cell to the bottom. Through the middle sections, as the plane of focus cuts through the nucleus, there was definite fluorescence staining in the nuclear compartment. This nuclear localization was critically dependent on the type of detergent used to permeabilize the cell: cells treated with saponin or digitonin yielded exclusively cytoplasmic staining while Triton X-100-treated cells showed nuclear as well as cytoplasmic labeling. Finally, double-immunofluorescence analysis showed that, within the nucleoplasm, the following pairs of nuclear antigens could be colocalized in certain speckled structures: (a) SC35 versus Sm; (b) galectin-1 versus Sm; (c) galectin-3 versus Sm; and (d) galectin-1 versus galectin-3. These results establish the presence of galectin-1 in the nuclei of HeLa cells, a conclusion consistent with the identification of the protein in nuclear extracts of the same cells and with its documentation as a factor in pre-mRNA splicing.

This paper focuses on extending the body of knowledge on co-creation in entrepreneurial contexts, by addressing the question of how entrepreneurs effect co-creation. In order to do so an inductive,...

Galectins are a family of beta-galactoside-binding proteins that contain characteristic amino acid sequences in the carbohydrate recognition domain (CRD) of the polypeptide. The polypeptide of galectin-1 contains a single domain, the CRD. The polypeptide of galectin-3 has two domains, a carboxyl-terminal CRD fused onto a proline- and glycine-rich amino-terminal domain. In previous studies, we showed that galectin-3 is a required factor in the splicing of nuclear pre-mRNA, assayed in a cell-free system. We now document that (i) nuclear extracts derived from HeLa cells contain both galectins-1 and -3; (ii) depletion of both galectins from the nuclear extract either by lactose affinity adsorption or by double-antibody adsorption results in a concomitant loss of splicing activity; (iii) depletion of either galectin-1 or galectin-3 by specific antibody adsorption fails to remove all of the splicing activity, and the residual splicing activity is still saccharide inhibitable; (iv) either galectin-1 or galectin-3 alone is sufficient to reconstitute, at least partially, the splicing activity of nuclear extracts depleted of both galectins; and (v) although the carbohydrate recognition domain of galectin-3 (or galectin-1) is sufficient to restore splicing activity to a galectin-depleted nuclear extract, the concentration required for reconstitution is greater than that of the full-length galectin-3 polypeptide. Consistent with these functional results, double-immunofluorescence analyses show that within the nucleus, galectin-3 colocalizes with the speckled structures observed with splicing factor SC35. Similar results are also obtained with galectin-1, although in this case, there are areas of galectin-1 devoid of SC35 and vice versa. Thus, nuclear galectins exhibit functional redundancy in their splicing activity and partition, at least partially, in the nucleoplasm with another known splicing factor.

We have compared the production of the related cytokines IL-13 and IL-4 by T lymphocytes, and the effects of the two cytokines on these cells. IL-13 and IL-4 production differ in a number of respects. IL-13 is produced at higher levels than IL-4 by activated T lymphocytes, and its accumulation in the culture medium can be more prolonged, corresponding partly to differential mRNA accumulation and partly to a preferential depletion of IL-4 from the culture medium. Certain inducing combinations such as PMA and anti-CD28, stimulate high levels of IL-13 and IL-13 mRNA, but little or no IL-4 or IL-4 mRNA. The ratio of IL-13 to IL-4, both at protein and mRNA levels, is higher in CD8+ lymphocyte than in CD4+ lymphocyte populations. Although after in vitro polarization of peripheral blood lymphocytes leading to type 1 and type 2 populations, IL-13 is made principally by cells of a type 2 phenotype, as is IL-4; it can also be produced by type 1 CD4+ and CD8+ T lymphocyte clones making large amounts of IFN-gamma and very little IL-4. IL-13 and IL-4 exert different effects on T lymphocyte functions. IL-13 does not significantly inhibit the IL-2-induced T lymphocyte production of IFN-gamma, RANTES, MIP-1 alpha or MIP-1 beta, nor that of perforin mRNA, as does IL-4. We have also been unable to demonstrate STAT6 activation by IL-13 on T lymphocytes purified in a number of ways, despite strong activation of STAT6 by IL-4 in these cells. This is contrary to some previous reports, but is consistent with the notion that the majority of T lymphocytes lack functional IL-13 receptors. A higher and more prolonged T lymphocyte production of IL-13 than that of IL-4 may thus be permissible because IL-13 does not inhibit T-cell functions. Conversely, sustained IL-13 production may be partly due to the absence of receptor-mediated depletion of this cytokine.

Introduction The protein ps20 encoded by the WFDC1 gene, is a member of a protein family containing conserved whey-4-disulphide-core (WFDC) domains. Ps20 is upregulated in prostate cancer epithelium and expression is thought to correlate with disease progression. The aim of this study was to determine whether ps20 expressed by prostate cancer cells also increases docetaxel resistance. Methods The cell-lines LNCaP and PC3 express low endogenous ps20, but were transfected with empty vector (EV) or WFDC1 gene vectors that increase WFDC1 RNA and ps20 protein expression by over 100% as measured by qPCR and ELISA. Docetaxel was added from 0.001nM –1µM with or without ps20 antibody (1G7) and cell-killing was assessed by MTT after 48 hours. Results EV-transfected PC3 and LNCaP cells have docetaxel IC50s of 0.223+/-0.05 and 0.16+/- 0.09nM respectively. In WFDC1-transfected PC3 and LNCAP, IC50s are increased to 0.677+/-0.11 and 0.326+/-0.05nM respectively (p Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4233. doi:1538-7445.AM2012-4233

Introduction The protein ps20 encoded by the WFDC1 gene contains a highly conserved whey 4-disulphide core (WFDC) domain and is a member of a protein family that regulates inflammation. Ps20/WFDC1 is expressed by prostate cancer stromal cells but its expression by cancerous prostate epithelium is associated with tumour progression in patients. The aim of this study was to determine how WFDC1expression by prostate cancer cells alters their tumourigenic properties. Methods The cell-lines LNCAP and PC3 were transfected with WFDC1 vector or empty vector (EV) and their growth, adhesive and migratory characteristics were investigated by MTT proliferation, transwell migration and ICAM-1 adhesion assays. Results PC3 and LNCAP cells transfected with WFDC1 increased in numbers by 3148 +/−151% and 523+/−311% after 48 hours respectively compared to EV transfected cell lines (p Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2833. doi:1538-7445.AM2012-2833

The H9 and CEM CD4+ T cell lines were infected with HIV-1 (NY5/LAV-1 isolate) and monitored for losses in cell viability, syncytium formation, and internucleosomal DNA cleavage (a marker for apoptosis). H9 cells were found to undergo cell death via apoptosis as a result of HIVNY5 infection, but this effect was not apparent in CEM cell cultures. The differential effects of HIV-1NY5 in terms of its apoptosis-inducing properties correlated with the relative abilities of H9 and CEM cells in supporting replication of this HIV-1 isolate, since infected CEM cell cultures produced 10-fold lower levels of HIV-1 p24 protein, and very few of these cells stained positive for cell-associated p24 by comparison with H9 cell cultures infected at the same multiplicity of infection. Furthermore, a different HIV-1 isolate (RF), which replicated equally efficiently in both H9 and CEM cells, produced similar levels of apoptosis in these cultures. HIV-1NY5 was also found to be capable of inducing apoptosis in purified peripheral blood CD4+ T cells as well as inhibiting anti-CD3-driven proliferation of these cells. In contrast, incubation of purified CD8+ T cells with HIV-1NY5 under similar conditions produced no cytopathic effects. Substantial levels of apoptosis were also recorded in HIV-1NY5-infected PHA blasts cell cultures. Soluble rHIV-1IIIB type CHO-derived gp120 was found to mimic the effects of HIV in terms of inhibition of anti-CD3/TCR mAb-induced proliferation of T cells, but apoptosis was not detected in gp120-treated T cell cultures whether cross-linked or used in conjunction with anti-CD3 mAb or not. We conclude therefore that both HIV-1NY5 and HIV-1RF isolates have the capacity to directly trigger apoptotic cell death in CD4+ T cells and that this appears to be at least partly associated with the efficiency of virus replication in these cells.