HIV-1 resistance to CCR5 antagonists associated with highly efficient use of CCR5 and altered tropism on primary CD4+ T cells
about
HIV-1 envelope-receptor interactions required for macrophage infection and implications for current HIV-1 cure strategiesBioinformatic analysis of HIV-1 entry and pathogenesis.A single-residue change in the HIV-1 V3 loop associated with maraviroc resistance impairs CCR5 binding affinity while increasing replicative capacity.Distinct HIV-1 entry phenotypes are associated with transmission, subtype specificity, and resistance to broadly neutralizing antibodies.Differences in coreceptor specificity contribute to alternative tropism of HIV-1 subtype C for CD4(+) T-cell subsets, including stem cell memory T-cellsCCR5 antibodies HGS004 and HGS101 preferentially inhibit drug-bound CCR5 infection and restore drug sensitivity of Maraviroc-resistant HIV-1 in primary cells.HIV-associated chronic immune activation.Chemokine receptor CCR5: from AIDS to atherosclerosisSelected amino acid mutations in HIV-1 B subtype gp41 are associated with specific gp120v₃ signatures in the regulation of co-receptor usage.HIV-1 escape from the CCR5 antagonist maraviroc associated with an altered and less-efficient mechanism of gp120-CCR5 engagement that attenuates macrophage tropismPhenotypic and immunologic comparison of clade B transmitted/founder and chronic HIV-1 envelope glycoproteins.Alternative coreceptor requirements for efficient CCR5- and CXCR4-mediated HIV-1 entry into macrophages.HIV-1 predisposed to acquiring resistance to maraviroc (MVC) and other CCR5 antagonists in vitro has an inherent, low-level ability to utilize MVC-bound CCR5 for entryHIV-1 clinical isolates resistant to CCR5 antagonists exhibit delayed entry kinetics that are corrected in the presence of drugDifferential use of CCR5 by HIV-1 clinical isolates resistant to small-molecule CCR5 antagonists.Transmitted/founder and chronic subtype C HIV-1 use CD4 and CCR5 receptors with equal efficiency and are not inhibited by blocking the integrin α4β7Vicriviroc resistance decay and relative replicative fitness in HIV-1 clinical isolates under sequential drug selection pressures.Affinofile profiling: how efficiency of CD4/CCR5 usage impacts the biological and pathogenic phenotype of HIVMacrophage-tropic HIV-1 variants from brain demonstrate alterations in the way gp120 engages both CD4 and CCR5HIV-1 pathogenesis: the virus.HIV-1 resistance to maraviroc conferred by a CD4 binding site mutation in the envelope glycoprotein gp120A common mechanism of clinical HIV-1 resistance to the CCR5 antagonist maraviroc despite divergent resistance levels and lack of common gp120 resistance mutationsMutations in variable domains of the HIV-1 envelope gene can have a significant impact on maraviroc and vicriviroc resistanceDecreased plasticity of coreceptor use by CD4-independent SIV Envs that emerge in vivo.Frequency and Env determinants of HIV-1 subtype C strains from antiretroviral therapy-naive subjects that display incomplete inhibition by maraviroc.Simultaneous zinc-finger nuclease editing of the HIV coreceptors ccr5 and cxcr4 protects CD4+ T cells from HIV-1 infection.Template-constrained cyclic sulfopeptide HIV-1 entry inhibitorsHIV-1 tropism testing and clinical management of CCR5 antagonists: Quebec review and recommendations.Quantifying susceptibility of CD4+ stem memory T-cells to infection by laboratory adapted and clinical HIV-1 strains.A mature macrophage is a principal HIV-1 cellular reservoir in humanized mice after treatment with long acting antiretroviral therapyDriving HIV-1 into a Vulnerable Corner by Taking Advantage of Viral Adaptation and Evolution.Increased stability and limited proliferation of CD4+ central memory T cells differentiate nonprogressive simian immunodeficiency virus (SIV) infection of sooty mangabeys from progressive SIV infection of rhesus macaques.Coreceptors and HIV-1 pathogenesis.Escape from human immunodeficiency virus type 1 (HIV-1) entry inhibitors.A maraviroc-resistant HIV-1 with narrow cross-resistance to other CCR5 antagonists depends on both N-terminal and extracellular loop domains of drug-bound CCR5Primary infection by a human immunodeficiency virus with atypical coreceptor tropismAdaptation of HIV-1 to cells with low expression of the CCR5 coreceptor.CCR5 receptor antagonists in preclinical to phase II clinical development for treatment of HIV.Quantifying CD4/CCR5 Usage Efficiency of HIV-1 Env Using the Affinofile System.Incompatible Natures of the HIV-1 Envelope in Resistance to the CCR5 Antagonist Cenicriviroc and to Neutralizing Antibodies.
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P2860
HIV-1 resistance to CCR5 antagonists associated with highly efficient use of CCR5 and altered tropism on primary CD4+ T cells
description
2010 nî lūn-bûn
@nan
2010 թուականի Ապրիլին հրատարակուած գիտական յօդուած
@hyw
2010 թվականի ապրիլին հրատարակված գիտական հոդված
@hy
2010年の論文
@ja
2010年論文
@yue
2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
@zh-tw
2010年论文
@wuu
name
HIV-1 resistance to CCR5 antag ...... ropism on primary CD4+ T cells
@ast
HIV-1 resistance to CCR5 antag ...... ropism on primary CD4+ T cells
@en
type
label
HIV-1 resistance to CCR5 antag ...... ropism on primary CD4+ T cells
@ast
HIV-1 resistance to CCR5 antag ...... ropism on primary CD4+ T cells
@en
prefLabel
HIV-1 resistance to CCR5 antag ...... ropism on primary CD4+ T cells
@ast
HIV-1 resistance to CCR5 antag ...... ropism on primary CD4+ T cells
@en
P2093
P2860
P50
P356
P1433
P1476
HIV-1 resistance to CCR5 antag ...... ropism on primary CD4+ T cells
@en
P2093
James F Demarest
Jennifer M Pfaff
John C Tilton
Robert W Doms
P2860
P304
P356
10.1128/JVI.00374-10
P407
P577
2010-04-21T00:00:00Z