HIV-1 escape from the CCR5 antagonist maraviroc associated with an altered and less-efficient mechanism of gp120-CCR5 engagement that attenuates macrophage tropism
about
HIV-1 envelope-receptor interactions required for macrophage infection and implications for current HIV-1 cure strategiesCurrent perspectives on HIV-1 antiretroviral drug resistanceHIV-1 gp120 as a therapeutic target: navigating a moving labyrinthAn inducible cell-cell fusion system with integrated ability to measure the efficiency and specificity of HIV-1 entry inhibitorsStructure and dynamics of the gp120 V3 loop that confers noncompetitive resistance in R5 HIV-1(JR-FL) to maravirocDendritic cell immunoreceptor is a new target for anti-AIDS drug development: identification of DCIR/HIV-1 inhibitorsCharacterizing the Diverse Mutational Pathways Associated with R5-Tropic Maraviroc Resistance: HIV-1 That Uses the Drug-Bound CCR5 Coreceptor.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.Longitudinal Analysis of CCR5 and CXCR4 Usage in a Cohort of Antiretroviral Therapy-Naïve Subjects with Progressive HIV-1 Subtype C Infection.Conformational alterations in the CD4 binding cavity of HIV-1 gp120 influencing gp120-CD4 interactions and fusogenicity of HIV-1 envelopes derived from brain and other tissuesAlternative coreceptor requirements for efficient CCR5- and CXCR4-mediated HIV-1 entry into macrophages.Covariance of charged amino acids at positions 322 and 440 of HIV-1 Env contributes to coreceptor specificity of subtype B viruses, and can be used to improve the performance of V3 sequence-based coreceptor usage prediction algorithms.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 entryCompartmentalization, Viral Evolution, and Viral Latency of HIV in the CNS.Differential use of CCR5 by HIV-1 clinical isolates resistant to small-molecule CCR5 antagonists.Vicriviroc 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 CCR5A common mechanism of clinical HIV-1 resistance to the CCR5 antagonist maraviroc despite divergent resistance levels and lack of common gp120 resistance mutationsThe HIV-1 env protein: a coat of many colors.Mutations in variable domains of the HIV-1 envelope gene can have a significant impact on maraviroc and vicriviroc resistanceLinkages between HIV-1 specificity for CCR5 or CXCR4 and in vitro usage of alternative coreceptors during progressive HIV-1 subtype C infection.Frequency and Env determinants of HIV-1 subtype C strains from antiretroviral therapy-naive subjects that display incomplete inhibition by maraviroc.Quantifying susceptibility of CD4+ stem memory T-cells to infection by laboratory adapted and clinical HIV-1 strains.Pre-exposure prophylaxis for HIV infection: how antiretroviral pharmacology helps to monitor and improve adherenceEffect of HIV-1 subtype and tropism on treatment with chemokine coreceptor entry inhibitors; overview of viral entry inhibition.Adaptation of HIV-1 to cells with low expression of the CCR5 coreceptor.HIV-1 susceptibility of transgenic rat-derived primary macrophage/T cells and a T cell line that express human receptors, CyclinT1 and CRM1 genes.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.Preclinical discovery and development of maraviroc for the treatment of HIV.V3 determinants of HIV-1 escape from the CCR5 inhibitors Maraviroc and Vicriviroc.Combination of the CCL5-derived peptide R4.0 with different HIV-1 blockers reveals wide target compatibility and synergic cobinding to CCR5Virus-cell fusion as a trigger of innate immunity dependent on the adaptor STING.Reduced Baseline Sensitivity to Maraviroc Inhibition Among R5 HIV-1 Isolates From Individuals With Severe Immunodeficiency.Unique Phenotypic Characteristics of Recently Transmitted HIV-1 Subtype C Envelope Glycoprotein gp120: Use of CXCR6 Coreceptor by Transmitted Founder Viruses.
P2860
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P2860
HIV-1 escape from the CCR5 antagonist maraviroc associated with an altered and less-efficient mechanism of gp120-CCR5 engagement that attenuates macrophage tropism
description
2011 nî lūn-bûn
@nan
2011 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
name
HIV-1 escape from the CCR5 ant ...... attenuates macrophage tropism
@ast
HIV-1 escape from the CCR5 ant ...... attenuates macrophage tropism
@en
type
label
HIV-1 escape from the CCR5 ant ...... attenuates macrophage tropism
@ast
HIV-1 escape from the CCR5 ant ...... attenuates macrophage tropism
@en
prefLabel
HIV-1 escape from the CCR5 ant ...... attenuates macrophage tropism
@ast
HIV-1 escape from the CCR5 ant ...... attenuates macrophage tropism
@en
P2093
P2860
P50
P356
P1433
P1476
HIV-1 escape from the CCR5 ant ...... attenuates macrophage tropism
@en
P2093
Anne Ellett
Becky Jubb
Filippo Posta
Martin R Jakobsen
Melissa J Churchill
Mike Westby
Paul R Gorry
P2860
P304
P356
10.1128/JVI.00106-11
P407
P577
2011-02-23T00:00:00Z