Invasive chronic inflammatory monocyte phenotype in subjects with high HIV-1 viral load.
about
Genetic, transcriptomic, and epigenetic studies of HIV-associated neurocognitive disorderUntangling the Gordian knot of HIV, stress, and cognitive impairmentHIV-1 infection of bone marrow hematopoietic progenitor cells and their role in trafficking and viral disseminationSialoadhesin ligand expression identifies a subset of CD4+Foxp3- T cells with a distinct activation and glycosylation profileA consensus surface activation marker signature is partially dependent on human immunodeficiency virus type 1 Nef expression within productively infected macrophagesTemporal dynamics of host molecular responses differentiate symptomatic and asymptomatic influenza a infection.Sialoadhesin (CD169) expression in CD14+ cells is upregulated early after HIV-1 infection and increases during disease progression.Sialoadhesin expressed on IFN-induced monocytes binds HIV-1 and enhances infectivity.Host hindrance to HIV-1 replication in monocytes and macrophages.Host genetic factors predisposing to HIV-associated neurocognitive disorder.Monocyte activation from interferon-α in HIV infection increases acetylated LDL uptake and ROS productionMonocyte activation in HIV/HCV coinfection correlates with cognitive impairment.Interferon-alpha drives monocyte gene expression in chronic unsuppressed HIV-1 infection.Sialoadhesin-deficient mice exhibit subtle changes in B- and T-cell populations and reduced immunoglobulin M levels.Antigen-specific interferon-gamma responses and innate cytokine balance in TB-IRISSuppressed monocyte gene expression profile in men versus women with PTSDHIV-1 immune activation induces Siglec-1 expression and enhances viral trans-infection in blood and tissue myeloid cells.Treatment intensification with maraviroc (CCR5 antagonist) leads to declines in CD16-expressing monocytes in cART-suppressed chronic HIV-infected subjects and is associated with improvements in neurocognitive test performance: implications for HIV-aShift in monocyte apoptosis with increasing viral load and change in apoptosis-related ISG/Bcl2 family gene expression in chronically HIV-1-infected subjects.JAM-A and ALCAM are therapeutic targets to inhibit diapedesis across the BBB of CD14+CD16+ monocytes in HIV-infected individuals.Breaking down the barrier: the effects of HIV-1 on the blood-brain barrier.Role of the immune system in HIV-associated neuroinflammation and neurocognitive implications.Monocytes mediate HIV neuropathogenesis: mechanisms that contribute to HIV associated neurocognitive disordersSIV encephalitis lesions are composed of CD163(+) macrophages present in the central nervous system during early SIV infection and SIV-positive macrophages recruited terminally with AIDS.Monocyte maturation, HIV susceptibility, and transmigration across the blood brain barrier are critical in HIV neuropathogenesisMacrophage colony stimulating factor regulation by nuclear factor kappa B: a relevant pathway in human immunodeficiency virus type 1 infected macrophages.Increased Expression of CD169 on Blood Monocytes and Its Regulation by Virus and CD8 T Cells in Macaque Models of HIV Infection and AIDS.Cognitive performance related to HIV-1-infected monocytesHIV-1 tuberculosis-associated immune reconstitution inflammatory syndromeCathepsin B and cystatin B in HIV-seropositive women are associated with infection and HIV-1-associated neurocognitive disorders.Effects of an exercise challenge on mobilization and surface marker expression of monocyte subsets in individuals with normal vs. elevated blood pressure.Transcriptome analysis reveals human cytomegalovirus reprograms monocyte differentiation toward an M1 macrophage.NeuroAIDS: characteristics and diagnosis of the neurological complications of AIDS.Antiretroviral therapy in HIV-1-infected individuals with CD4 count below 100 cells/mm3 results in differential recovery of monocyte activation.Effect of cytokines on Siglec-1 and HIV-1 entry in monocyte-derived macrophages: the importance of HIV-1 envelope V1V2 regionBasic and clinical immunology of SiglecsTranscriptome analysis of HIV-infected peripheral blood monocytes: gene transcripts and networks associated with neurocognitive functioning.Circulating monocytes in HIV-1-infected viremic subjects exhibit an antiapoptosis gene signature and virus- and host-mediated apoptosis resistance.Transcriptome analysis of primary monocytes from HIV-positive patients with differential responses to antiretroviral therapy.Host Immune Responses in HIV-1 Infection: The Emerging Pathogenic Role of Siglecs and Their Clinical Correlates.
P2860
Q26865707-8C94F277-7B8D-47E0-A3C6-493A63CCCA00Q28067483-DD73CA17-9059-4E80-BAFF-A4B8FD58ADEAQ28474374-90941ECF-DBF0-4016-B288-793B9FD7F1A1Q28509206-57BC9F2F-0BCC-4703-A0A1-D1F9D8A9176CQ30009511-A5BAE00C-E6F7-4266-9859-BB2D32DE1C6FQ30406849-355454FE-BE8F-4BE7-BB68-59ADFBFD86B9Q33276138-8AA84204-814A-4170-B65F-4B8FE8D3A4D3Q33328484-8D39A34D-E658-4692-85DE-D239484965CAQ33846376-54B4C7BB-8A62-4407-B86A-7EA46E8D1FF0Q34001122-9189424D-4EA0-4B53-A4D7-9445A9B0AF48Q34292033-BD73087A-9AE9-4E7B-B0F3-9E6CF5BC4E5BQ34329530-F01FB3AB-614E-43B5-9991-7D17C4FEF9BEQ34346743-1E424299-7D0A-47C6-A87A-6CF0E6870DE8Q34353668-BEE4A1AB-23AB-4EFC-A62E-6BD320EC9DECQ34557159-D86E9CDB-7EE7-42CC-A1DB-E87781B90A5DQ34574560-437293B7-BF7B-4B4B-9667-9322A5E71CCDQ34669697-0CF0C27E-ACBB-4301-9546-1F4316DC9C99Q34718135-8B923C73-506B-44DE-8B2D-3F55BB04131EQ34992712-2C7C8674-EE0A-45C5-AE26-5CAA8466CE8FQ35005863-97557409-47D8-42A4-8FA2-8AAB26AC694AQ35114694-91BA3794-C62F-4DD3-AE3F-35B874F3CC99Q35125996-460BF3D3-8F8D-42FB-9ABC-8D8E19CA4849Q35154529-877CFAB3-C678-41D1-AB5A-3208F33767A4Q35669020-D6916A15-FCC6-4B74-A32E-687CEA2C9029Q35787684-109B95AB-29B6-4336-A3F4-F3466130B7A0Q35823900-B998DEA1-7964-44BC-82C7-CDE5ECCE2F0EQ35861507-9376F6AC-9523-41EC-909B-06F95CCA4D12Q35909507-1433A406-B844-4E16-ADAD-B62203936F41Q36654015-0B848116-7099-4C70-BE91-8BF3E350E186Q36670527-7B313D98-F63E-406D-AF12-87CAA73DDB58Q36792699-88A390F7-E81E-493C-BC31-914C07F93BA9Q37040044-D67EDD01-51D5-42F5-B652-C0EAD69C762BQ37089861-AF161ECB-CEDF-41F7-B84B-F779DD877956Q37098066-50F02616-EF1D-419F-B893-FC5E4094585DQ37111282-72579985-2FAF-401E-AC3C-6092BA79B4B2Q37348437-865409CB-1437-4CE5-AD57-EFFE8D170EF2Q37374036-C9FCD3D1-40DA-44CC-80FC-382770D46364Q37418469-88E791D8-BEAE-42A0-8DE6-5C32CF1B3B6BQ37425190-20F5175B-A124-4533-BBB3-A7D7458D5078Q37716750-C665FF1F-47BF-45D7-BB59-5CCD0A8ADEEC
P2860
Invasive chronic inflammatory monocyte phenotype in subjects with high HIV-1 viral load.
description
2004 nî lūn-bûn
@nan
2004年の論文
@ja
2004年学术文章
@wuu
2004年学术文章
@zh
2004年学术文章
@zh-cn
2004年学术文章
@zh-hans
2004年学术文章
@zh-my
2004年学术文章
@zh-sg
2004年學術文章
@yue
2004年學術文章
@zh-hant
name
Invasive chronic inflammatory monocyte phenotype in subjects with high HIV-1 viral load.
@en
Invasive chronic inflammatory monocyte phenotype in subjects with high HIV-1 viral load.
@nl
type
label
Invasive chronic inflammatory monocyte phenotype in subjects with high HIV-1 viral load.
@en
Invasive chronic inflammatory monocyte phenotype in subjects with high HIV-1 viral load.
@nl
prefLabel
Invasive chronic inflammatory monocyte phenotype in subjects with high HIV-1 viral load.
@en
Invasive chronic inflammatory monocyte phenotype in subjects with high HIV-1 viral load.
@nl
P2093
P1476
Invasive chronic inflammatory monocyte phenotype in subjects with high HIV-1 viral load.
@en
P2093
Hans Rempel
Lynn Pulliam
P356
10.1016/J.JNEUROIM.2004.08.039
P577
2004-12-01T00:00:00Z