Lista de obras - Michael Roche - Dominio Público Uruguay

A common mechanism of clinical HIV-1 resistance to the CCR5 antagonist maraviroc despite divergent resistance levels and lack of common gp120 resistance mutations

artículo científico publicado en 2013

Alternative coreceptor requirements for efficient CCR5- and CXCR4-mediated HIV-1 entry into macrophages

artículo científico publicado en 2011

An altered and more efficient mechanism of CCR5 engagement contributes to macrophage tropism of CCR5-using HIV-1 envelopes

artículo científico publicado en 2010

Analysis of clinical HIV-1 strains with resistance to maraviroc reveals strain-specific resistance mutations, variable degrees of resistance, and minimal cross-resistance to other CCR5 antagonists.

artículo científico publicado en 2017

Asn 362 in gp120 contributes to enhanced fusogenicity by CCR5-restricted HIV-1 envelope glycoprotein variants from patients with AIDS.

artículo científico publicado en 2007

CD4-binding site alterations in CCR5-using HIV-1 envelopes influencing gp120-CD4 interactions and fusogenicity

artículo científico publicado en 2011

Enhanced CD4+ cellular apoptosis by CCR5-restricted HIV-1 envelope glycoprotein variants from patients with progressive HIV-1 infection

artículo científico publicado en 2009

HIV-1 and SIV Predominantly Use CCR5 Expressed on a Precursor Population to Establish Infection in T Follicular Helper Cells

artículo científico publicado en 2017

HIV-1 entry and trans-infection of astrocytes involves CD81 vesicles.

artículo científico publicado en 2014

HIV-1 escape from the CCR5 antagonist maraviroc associated with an altered and less-efficient mechanism of gp120-CCR5 engagement that attenuates macrophage tropism

artículo científico publicado en 2011

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 entry

artículo científico publicado en 2011

Impact of alemtuzumab on HIV persistence in an HIV-infected individual on antiretroviral therapy with Sezary syndrome.

artículo científico publicado en 2017

Is the central nervous system a reservoir of HIV-1?

artículo científico publicado en 2014

Linkages between HIV-1 specificity for CCR5 or CXCR4 and in vitro usage of alternative coreceptors during progressive HIV-1 subtype C infection

artículo científico publicado en 2013

Longitudinal Analysis of CCR5 and CXCR4 Usage in a Cohort of Antiretroviral Therapy-Naïve Subjects with Progressive HIV-1 Subtype C Infection.

artículo científico publicado en 2013

Longitudinal analysis of subtype C envelope tropism for memory CD4+ T cell subsets over the first 3 years of untreated HIV-1 infection

artículo científico publicado en 2020

Macrophage-tropic HIV-1 variants from brain demonstrate alterations in the way gp120 engages both CD4 and CCR5

artículo científico publicado en 2012

Molecular Gymnastics: Mechanisms of HIV-1 Resistance to CCR5 Antagonists and Impact on Virus Phenotypes

artículo científico

Pathogenicity and immunogenicity of attenuated, nef-deleted HIV-1 strains in vivo

artículo científico publicado en 2007

Pembrolizumab induces HIV latency reversal in people living with HIV and cancer on antiretroviral therapy

artículo científico publicado en 2022

Quantifying susceptibility of CD4+ stem memory T-cells to infection by laboratory adapted and clinical HIV-1 strains

artículo científico publicado en 2014

Reliable genotypic tropism tests for the major HIV-1 subtypes

artículo científico publicado en 2015

Site-selective solid-phase synthesis of a CCR5 sulfopeptide library to interrogate HIV binding and entry

artículo científico publicado en 2014

The NRTIs lamivudine, stavudine and zidovudine have reduced HIV-1 inhibitory activity in astrocytes

artículo científico publicado en 2013

The magnitude of HIV-1 resistance to the CCR5 antagonist maraviroc may impart a differential alteration in HIV-1 tropism for macrophages and T-cell subsets

artículo científico publicado en 2013

Tissue-specific sequence alterations in the human immunodeficiency virus type 1 envelope favoring CCR5 usage contribute to persistence of dual-tropic virus in the brain

artículo científico publicado en 2009

Variation in cell-associated unspliced HIV RNA on antiretroviral therapy is associated with the circadian regulator brain-and-muscle-ARNT-like-1

artículo científico publicado en 2018

X4 and R5 HIV-1 have distinct post-entry requirements for uracil DNA glycosylase during infection of primary cells

artículo científico publicado en 2010

i-bodies, Human Single Domain Antibodies That Antagonize Chemokine Receptor CXCR4.

artículo científico publicado en 2016

Lista de obras de Michael Roche

A common mechanism of clinical HIV-1 resistance to the CCR5 antagonist maraviroc despite divergent resistance levels and lack of common gp120 resistance mutations

Alternative coreceptor requirements for efficient CCR5- and CXCR4-mediated HIV-1 entry into macrophages

An altered and more efficient mechanism of CCR5 engagement contributes to macrophage tropism of CCR5-using HIV-1 envelopes

Analysis of clinical HIV-1 strains with resistance to maraviroc reveals strain-specific resistance mutations, variable degrees of resistance, and minimal cross-resistance to other CCR5 antagonists.

Asn 362 in gp120 contributes to enhanced fusogenicity by CCR5-restricted HIV-1 envelope glycoprotein variants from patients with AIDS.

CD4-binding site alterations in CCR5-using HIV-1 envelopes influencing gp120-CD4 interactions and fusogenicity

Enhanced CD4+ cellular apoptosis by CCR5-restricted HIV-1 envelope glycoprotein variants from patients with progressive HIV-1 infection

HIV-1 and SIV Predominantly Use CCR5 Expressed on a Precursor Population to Establish Infection in T Follicular Helper Cells

HIV-1 entry and trans-infection of astrocytes involves CD81 vesicles.

HIV-1 escape from the CCR5 antagonist maraviroc associated with an altered and less-efficient mechanism of gp120-CCR5 engagement that attenuates macrophage tropism

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 entry

Impact of alemtuzumab on HIV persistence in an HIV-infected individual on antiretroviral therapy with Sezary syndrome.

Is the central nervous system a reservoir of HIV-1?

Linkages between HIV-1 specificity for CCR5 or CXCR4 and in vitro usage of alternative coreceptors during progressive HIV-1 subtype C infection

Longitudinal Analysis of CCR5 and CXCR4 Usage in a Cohort of Antiretroviral Therapy-Naïve Subjects with Progressive HIV-1 Subtype C Infection.

Longitudinal analysis of subtype C envelope tropism for memory CD4+ T cell subsets over the first 3 years of untreated HIV-1 infection

Macrophage-tropic HIV-1 variants from brain demonstrate alterations in the way gp120 engages both CD4 and CCR5

Molecular Gymnastics: Mechanisms of HIV-1 Resistance to CCR5 Antagonists and Impact on Virus Phenotypes

Pathogenicity and immunogenicity of attenuated, nef-deleted HIV-1 strains in vivo

Pembrolizumab induces HIV latency reversal in people living with HIV and cancer on antiretroviral therapy

Quantifying susceptibility of CD4+ stem memory T-cells to infection by laboratory adapted and clinical HIV-1 strains

Reliable genotypic tropism tests for the major HIV-1 subtypes

Site-selective solid-phase synthesis of a CCR5 sulfopeptide library to interrogate HIV binding and entry

The NRTIs lamivudine, stavudine and zidovudine have reduced HIV-1 inhibitory activity in astrocytes

The magnitude of HIV-1 resistance to the CCR5 antagonist maraviroc may impart a differential alteration in HIV-1 tropism for macrophages and T-cell subsets

Tissue-specific sequence alterations in the human immunodeficiency virus type 1 envelope favoring CCR5 usage contribute to persistence of dual-tropic virus in the brain

Variation in cell-associated unspliced HIV RNA on antiretroviral therapy is associated with the circadian regulator brain-and-muscle-ARNT-like-1

X4 and R5 HIV-1 have distinct post-entry requirements for uracil DNA glycosylase during infection of primary cells

i-bodies, Human Single Domain Antibodies That Antagonize Chemokine Receptor CXCR4.