about
Activation of HIV transcription with short-course vorinostat in HIV-infected patients on suppressive antiretroviral therapyReduced hepatitis B virus (HBV)-specific CD4+ T-cell responses in human immunodeficiency virus type 1-HBV-coinfected individuals receiving HBV-active antiretroviral therapy.No increase in hepatitis B virus (HBV)-specific CD8+ T cells in patients with HIV-1-HBV coinfections following HBV-active highly active antiretroviral therapy.Entinostat is a histone deacetylase inhibitor selective for class 1 histone deacetylases and activates HIV production from latently infected primary T cells.Coinfection of hepatic cell lines with human immunodeficiency virus and hepatitis B virus leads to an increase in intracellular hepatitis B surface antigen.Establishment of HIV-1 latency in resting CD4+ T cells depends on chemokine-induced changes in the actin cytoskeleton.Ex vivo response to histone deacetylase (HDAC) inhibitors of the HIV long terminal repeat (LTR) derived from HIV-infected patients on antiretroviral therapy.Effect of ipilimumab on the HIV reservoir in an HIV-infected individual with metastatic melanoma.Understanding Factors That Modulate the Establishment of HIV Latency in Resting CD4+ T-Cells In Vitro.Altering cell death pathways as an approach to cure HIV infection.HDAC inhibitors in HIV.HIV reservoirs and strategies for eradication.Comparison of sequence analysis and a novel discriminatory real-time PCR assay for detection and quantification of Lamivudine-resistant hepatitis B virus strains.The novel histone deacetylase inhibitors metacept-1 and metacept-3 potently increase HIV-1 transcription in latently infected cells.Highly reproducible transient transfections for the study of hepatitis B virus replication based on an internal GFP reporter system.Comparison of HDAC inhibitors in clinical development: effect on HIV production in latently infected cells and T-cell activation.Both CD31(+) and CD31⁻ naive CD4(+) T cells are persistent HIV type 1-infected reservoirs in individuals receiving antiretroviral therapy.Severe hepatitis and prolonged hepatitis B virus-specific CD8 T-cell response after selection of hepatitis B virus YMDD variant in an HIV/hepatitis B virus-co-infected patient.The phenotype of hepatitis B virus-specific T cells differ in the liver and blood in chronic hepatitis B virus infection.Enhanced replicative capacity and pathogenicity of HIV-1 isolated from individuals infected with drug-resistant virus and declining CD4+ T-cell counts.Virologic determinants of success after structured treatment interruptions of antiretrovirals in acute HIV-1 infection.CCR7 ligands CCL19 and CCL21 increase permissiveness of resting memory CD4+ T cells to HIV-1 infection: a novel model of HIV-1 latency.
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description
researcher ORCID ID = 0000-0003-1203-1325
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wetenschapper
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name
Fiona Wightman
@ast
Fiona Wightman
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Fiona Wightman
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Fiona Wightman
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type
label
Fiona Wightman
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Fiona Wightman
@en
Fiona Wightman
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Fiona Wightman
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prefLabel
Fiona Wightman
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Fiona Wightman
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Fiona Wightman
@es
Fiona Wightman
@nl
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P1153
7003849998
P31
P496
0000-0003-1203-1325