Viewing negative mentions of gene expression of HIVEP1 (H. sapiens) in T cells

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Wilson et al. (2000)HIVT cellsIn contrast, HIV-1-specific proliferative responses were absent in most individuals with progressive HIV-1 infection, even though interferon-gamma-producing HIV-1-specific CD4(+) T cells were detectable by flow cytometry.
Bartz and Emerman (1999)HIV-1T cellsWe found that HIV-1 lacking the env gene (HIVDeltaenv) still induced apoptosis in T-cell lines and primary CD4 T cells.
Schmökel et al. (2009)HIV-1T cellIn agreement with these previous results, the about 5-fold increase in the expression levels of the early T cell activation marker CD69 upon PHA stimulation was blocked in PBMC infected with the HIV-1 construct expressing the 239 wt Nef but not in those expressing the HIV-1 NL4-3 or NA7 Nef proteins (Fig. 5A, panels 2–4).
Langlois et al. (2005)HIV-1T-cellvif HIV-1 can be propagated in CEM-SS cells (a permissive T-cell line) but not in the non-permissive CEM progenitor (1).
Rasheed et al. (2009)HIVT-cellsThe VEGF ligand and its cognate receptor VEGFR were not detected in the experimentally HIV-infected T-cells tested over a period of two years.
Hersperger et al. (2010)HIVT-cellsIndeed, some HIV-specific CD8+ T-cells in both EC and CP were CD27-CD45RO- yet did not express perforin.
Herasimtschuk et al. (2008)HIV-1T-cellWhile patients maintained a stable population of cells, at baseline a complete lack of both CD4+ and CD8+ HIV-1-specific T-cell responses was noted in 11 of 12 individuals.
Henriet et al. (2007)HIV-1T-cellIn particular, Vif is required for efficient HIV-1 replication in so called ‘non-permissive’ cells such as primary CD4+T lymphocytes and macrophages and some T-cell lines (H9, HUT78), whereas HIV-1 lacking vif (HIV-1?
Jacobson et al. (2009)HIVT cellsT cell activation is also consistently higher in antiretroviral-suppressed patients compared to HIV negatives, and when present is often associated with suboptimal gains in absolute CD4+ T cells.
Lubong Sabado et al. (2009)HIVT cellIn particular, Env-specific CD4+ T cell responses, which are not commonly detected in chronic HIV-infected subjects, are readily detected during AHI.
Phipps et al. (1997)HIV-1T-cellWe determined the relative specific kinase activity of Fyn in lysates of peripheral blood mononuclear cells from 47 normal control individuals tested negative for HIV-1 and -2, human T-cell lymphotropic virus Type I, hepatitis B virus (HBV), hepatitis C virus (HCV), and syphilis; 14 asymptomatic HIV-infected patients having near-normal CD4+ T-cell counts (350 to 980 CD4+ cells/microL); 4 patients with symptomatic acquired immunodeficiency syndrome (AIDS) (<30 CD4+ cells/microL); 13 patients having chronic infection with HBV (6 patients) or HCV (7 patients); and 6 patients with systemic lupus erythematosis (SLE).
Lehmann et al. (2008)HIV-RNAT-cellsThe NA for regimen consisted of atazanavir (300 mg qd), saquinavir (1000 mg bid), and ritonavir (100mg qd) in 14 patients with immunologic failure despite undetectable plasma HIV-RNA (CD4(+) T-cells < 250 cells/microL (<17%) HIV RNA, <= 50 copies/mL).
Chaipan et al. (2010)HIV-1T-cellsPodoplanin is not expressed on HIV-1 infected T-cells
Chaipan et al. (2010)HIVT-cellAnalysis of T-cell lines and PBMCs for podoplanin expression yielded negative results (Fig. 5), at least when viable cells were analyzed (see below), indicating that HIV particles generated in patients might not harbour podoplanin.
Chaipan et al. (2010)HIVT-cellsPodoplanin was not expressed on viable T-cells, the major HIV target cell, and might thus be of minor importance for viral spread in vivo.
Lassen et al. (2006)HIV-1T cellsResting CD4+ T cells from patients on HAART do not spontaneously produce HIV-1 unless activated [4,10].
Yu et al. (2008)HIVT cellHIV Traffics through a Specialized, Surface-Accessible Intracellular Compartment during trans-Infection of T Cells by Mature Dendritic Cells In vitro, dendritic cells (DCs) bind and transfer intact, infectious HIV to CD4 T cells without first becoming infected, a process known as trans-infection. trans-infection is accomplished by recruitment of HIV and its receptors to the site of DC–T cell contact and transfer of virions at a structure known as the infectious synapse.
Neuenburg et al. (2004)HIV-1T cellsWe found that most CSF T cells were not HIV-1 producing, even when cell-free viral load in CSF was high.
Soros et al. (2007)HIVT cellsAPOBEC3G (A3G) is a highly active antiretroviral deoxycytidine deaminase that greatly impairs HIV spread in cultures of activated CD4 T cells provided the HIV Vif protein is absent [1].
Sakata et al. (1990)NKH-1-positiveT cellThis disease include T-GL having CD3 antigen which forms a complex with T cell Ag receptor (TCR-alpha beta), and NK-GL which is CD3-negative but CD16- or NKH-1-positive, having non-MHC-restricted cytotoxicity.