GB virus C: Insights into co-infection

Berzsenyi, Mark D.; Bowden, D. Scott; Roberts, Stuart K.

doi:10.1016/j.jcv.2005.04.002

Cited by 42 publications

(47 citation statements)

References 87 publications

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“…Epidemiological studies have indicated that it does not cause acute or chronic hepatitis [1][2][3][4]. In recent years numerous studies have been published in which coinfection with GBV-C/HGV and the human immunodeficiency virus (HIV) have been associated with slower progression of the illness and a higher survival rate of patients once AIDS has developed [5][6][7]. The mechanism responsible for the beneficial effect that the GBV-C/HGV virus has on the course of infection caused by HIV has not been defined.…”

Section: Introductionmentioning

confidence: 99%

Liposome destabilization induced by synthetic lipopeptides corresponding to envelope and non-structural domains of GBV-C/HGV virus. Conformational requirements for leakage

Fernández-Vidal

Rojo

Herrera

et al. 2008

Biophysical Chemistry

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Liposome destabilization induced by synthetic lipopeptides corresponding to envelope and non-structural domains of gbv-c/hgv virus. conformational requirements for leakage, Biophysical Chemistry (2007Chemistry ( ), doi: 10.1016Chemistry ( /j.bpc.2007 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A C C E P T E D M A N U S C R I P T ACCEPTED MANUSCRIPT LIPOSOME DESTABILIZATION INDUCED BY SYNTHETIC LIPOPEPTIDES CORRESPONDING TO ENVELOPE AND NON-STRUCTURAL DOMAINS OF GBV-C/HGV VIRUS. CONFORMATIONAL REQUIREMENTS FOR LEAKAGE A C C E P T E D M A N U S C R I P T ACCEPTED MANUSCRIPT 2 AbstractLiposomes have been used primarily as a model system for studying biological membranes.

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Section: Introductionmentioning

confidence: 99%

Liposome destabilization induced by synthetic lipopeptides corresponding to envelope and non-structural domains of GBV-C/HGV virus. Conformational requirements for leakage

Fernández-Vidal

Rojo

Herrera

et al. 2008

Biophysical Chemistry

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“…cells (PBMC), including CD4 positive T cells (2). GBV-C co-infection has been recently proposed to have a beneficial effect on HIV disease course, since slower disease progression and enhanced survival has been observed in GBV-C-positive as compared to GBV-C-negative subjects (3)(4).…”

mentioning

confidence: 99%

Activation of Interferon Response Genes and of Plasmacytoid Dendritic Cells in HIV-1 Positive Subjects with GB Virus C Co-Infection

Lalle

Sacchi

Abbate

et al. 2008

Int J Immunopathol Pharmacol

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GB virus C (GBV-C) coinfection has a protective role in Human Immunodeficiency Virus (HIV) infection, and increases the duration of suppression of HIV-1 viremia in patients under Highly Active Anti-Retroviral Therapy (HAART). Since innate antiviral response may be involved in the protection, we analyzed the possible role of GBV-C as activator of innate immunity. To this aim, we measured the extent of activation of the interferon (IFN) system and of circulating Dendritic Cells (DC) in vivo, and the ability of GBV-C to activate these functions in vitro. Activation of IFN system and of circulating DC was compared in GBV-positive and -negative HIV-1 co-infected patients with HAART-driven suppression of HIV-1 viremia. Endogenous levels of IFN-γ and RNA-dependent protein kinase (PKR) mRNA were significantly higher in peripheral blood mononuclear cells (PBMC) from GBV-C-positive when compared to GBV-C-negative patients. IFN-γ expression was correlated with all the Interferon response genes (IRGs) and with GBV-C viremia. The frequency of circulating plasmacytoid DC (pDC) expressing the CD80 activation marker was increased in GBV-C-positive patients, and was correlated with GBV-C viral load. In vitro experiments indicated that GBV-C is able to induce IFN-γ expression in PBMC. In addition, in PBMC cultures GBV-C induced an increase of CD80 expression by pDC, that was reduced by antibody to IFN-γ. Our data indicate that in HIV-positive patients GBV-C coinfection promotes the activation of IFN-γ and downstream IRG expression, as well as with the activation/maturation of circulating pDC. GBV-C-driven IFN-γ activation is, at least in part, responsible for the increased maturation of pDC. This crosstalk may suggest a role for GBV-C coinfection in boosting the innate antiviral response to HIV infection.

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“…Por otro lado, estudios in vitro muestran la inhibición de la replicación tanto de cepas R5 como X4 por parte del GBV-C, utilizando como marcador los niveles del antígeno p24 29 . Aunque es cuestión de debate, existen estudios sero-epidemiológicos y de cohorte con resultados contradictorios, en los que se concluye que la co-infección no se asocia con beneficio en el desenlace clínico de los pacientes 4,30,31 . Es el caso de un estudio de cohorte que involucró 18 mujeres de origen africano infectadas con el VIH-1 o el VIH-2 y co-infectadas por el GBV-C. En este trabajo no se observaron diferencias en la carga viral de VIH o en los recuentos de CD4, ni en la mortalidad de las mujeres co-infectadas, en comparación con las no co-infectadas.…”

Section: Co-infección Gbv-c/vihunclassified

“…También se demostró que la co-infección GBV-C/VIH-1 en individuos con enfermedad avanzada se asocia con una baja expresión de los co-receptores CCR5 y CXCR4 en la membrana de linfocitos T CD4+ 37 . Análisis in vitro describen que estas quimioquinas son capaces de inhibir la infección por el VIH 4,35 , proponiéndose dos modelos para este efecto (Figura 3A). En el primero, las quimioquinas se unen al dominio de unión del co-receptor (CXCR4 o CCR5) que interactúa con gp120, causando un impedimento estérico que afecta la entrada del VIH a las células blanco.…”

Section: Inmunomodulación Por El Gbv-cunclassified

“…En años posteriores, algunos estudios serían realizados para tratar de establecer factores de riesgo en pacientes con enfermedad hepática, sin resultados concluyentes que permitan asociar al GBV-C con hepatopatía 1 . Por el contrario, trabajos epidemiológicos y experimentales adelantados en la última década han vinculado al GBV-C con la inhibición del virus de la inmunodeficiencia humana tipo 1 (VIH-1) en el contexto de co-infección, afectando favorablemente la evolución clínica y retrasando el progreso a SIDA (síndrome de inmunodeficiencia humana) 4 . En esta revisión se destacan los principales estudios clínicos acerca de la co-infección GBV-C/VIH y las evidencias in vitro que soportan el efecto inhibitorio sobre la replicación de VIH-1 mediado principalmente por las proteínas E1, E2, NS3 y NS5A del virus GB tipo C 5 .…”

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Interacción entre el virus de la inmunodeficiencia humana y el virus GB tipo-C durante el estado de co-infección

Arroyave

Pujol

Navas

et al. 2013

Rev. chil. infectol.

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GB virus C: Insights into co-infection

Cited by 42 publications

References 87 publications

Liposome destabilization induced by synthetic lipopeptides corresponding to envelope and non-structural domains of GBV-C/HGV virus. Conformational requirements for leakage

Liposome destabilization induced by synthetic lipopeptides corresponding to envelope and non-structural domains of GBV-C/HGV virus. Conformational requirements for leakage

Activation of Interferon Response Genes and of Plasmacytoid Dendritic Cells in HIV-1 Positive Subjects with GB Virus C Co-Infection

Interacción entre el virus de la inmunodeficiencia humana y el virus GB tipo-C durante el estado de co-infección

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