Plasma HCV‐RNA decline in the first 48 h identifies hepatitis C virus mono‐infected but not HCV/HIV‐coinfected patients with an undetectable HCV viral load at week 4 of peginterferon‐alfa‐2a/ribavirin therapy
Department of Internal Medicine and Infectious Diseases, University Medical Center Utrecht, Utrecht, The Netherlands. Journal of Viral Hepatitis
(Impact Factor: 3.91).
06/2009; 16(12):867-75. DOI: 10.1111/j.1365-2893.2009.01143.x
During peginterferon-alfa-2a/ribavirin therapy, plasma hepatitis C virus (HCV)-RNA decreases with a rapid first phase and a slower second phase. We compared the viral load decrease and slope in the first 48 h in patients with a rapid viral response (RVR, i.e. HCV-RNA < 50 IU/mL at week 4) with patients not achieving an RVR. From 23 HCV-infected (14 mono-infected and nine HCV/HIV-coinfected) genotype 1 or 4 positive peginterferon-alfa-2a/ribavirin-treated patients, plasma HCV-RNA was determined at baseline, 48 h, weeks 1, 2, 4, 8, 12, 48 and 72. The HCV viral load decrease (Delta0-48), the slope (lambda(1)) and the efficiency factor (epsilon) were determined in the first 48 h after the start of therapy. Five (36%) HCV mono-infected patients and three (33%) HIV/HCV-coinfected patients achieved an RVR whereas six (43%) HCV mono-infected patients and five (56%) HIV/HCV-coinfected patients reached a sustained viral response (SVR). In contrast to HIV/HCV-coinfected patients, five HCV mono-infected patients with an RVR showed both a larger Delta0-48 and steeper lambda(1) (-1.77log(10) IU/mL +/- 0.66 and -2.04/day +/- 0.76) compared to nine non-RVR patients (-0.66log(10) IU/mL +/- 0.39; P = 0.019 and -0.76/day +/- 0.41; P = 0.019). When divided by SVR, a greater Delta0-48 and steeper lambda(1) were also seen in both HCV mono-infected and HIV/HCV-coinfected patients. Thus, in the first 48 h after the start of therapy, HCV mono-infected patients with an RVR have a larger viral load decrease, steeper viral slope and a higher efficiency factor as compared with non-RVR patients.
Figures in this publication
Available from: Cristiano Alicino
- "These findings are consistent with those from Arends et al. in which patients, infected with HCV genotype 1 and 4, that experienced a rapid decline of viral load at 48 hour (median 1.77 log) achieve RVR. This correlation has been reported only for mono-infected subjects . In the setting of mono-infection HCV, the study of Durante-Mangoni et al., including 119 patients, "
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ABSTRACT: Rapid virological response (RVR) is a critical end-point in the era of the new direct-acting antiviral agents (DAA). The aim of this study was to evaluate the predictive value in achieving RVR of HCV-RNA load and IP10 after 48hours of standard anti HCV therapy.
HCV mono-infected and HIV/HCV co-infected patients naives to interferon were included. Demographic data, immune-virological HIV-related condition and HCV disease status were recorded before starting treatment. HCV-RNA and IP10 concentrations were also measured 48hours after first interferon dose. Univariate model, logistic regression and ROC curve were performed for statistical analysis.
Thirty-two patients were enrolled (mean age 49.2±5.6 years): all were treated with pegylated-interferon and ribavirin. Nineteen (59.3%) were HIV/HCV co-infected patients. RVR was reached in 10 patients (31.2%). A decline of more than two log of HCV-RNA after 48hours of therapy was associated with RVR (P=0.004). A trend was observed between increased IP10 levels at 48hours and RVR (P=0.08). In a multivariable model only HCV-RNA at 48hours was associated with RVR (P=0.011). ROC curve analysis for both HCV-RNA at 48hours and IP-10 at 48hours showed an area under the curve of 0.87 (95%CI: 0.74-1; P=0.001) with specificity of 72.2% and sensibility of 90%.
In HCV treatment-naïve patients HCV-RNA and IP10 determination after 48hours of interferon and ribavirin may be a worthwhile endpoint to predict RVR and select patients that may not require DAA addition.
Copyright © 2015 Elsevier Masson SAS. All rights reserved.
Gastroentérologie Clinique et Biologique 06/2015; DOI:10.1016/j.clinre.2015.04.001 · 1.64 Impact Factor
Available from: archives-ouvertes.fr
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ABSTRACT: A novel OMCVD process for the highly selective deposition of pure,
adherent, low resistivity copper films onto conductive substrates is
described. Central to this process is a new volatile liquid
copper<sup>+1</sup> precursor, Cupra Select, designed to thermally
disproportionate at low temperatures to cleanly give copper metal and
volatile non-corrosive by-products. Thus, selective depositions onto
metallic versus insulating dielectric substrates are achieved between
120 to 420°C with growth rates in excess of 100 nm/min and grain
sizes as low as 0.1 microns. In addition, a novel complementary copper
etching process is discussed that is chemically compatible with the
copper CVD chemistry
VLSI Multilevel Interconnection Conference, 1991, Proceedings., Eighth International IEEE; 07/1991
Available from: Debbie van Baarle
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ABSTRACT: The aim of this study was to study the development of HCV-specific T cell immunity during acute HCV infection in the presence of an existing HIV-1 infection in four HIV-1 infected men having sex with men. A comprehensive analysis of HCV-specific T cell responses was performed at two time points during acute HCV infection using a T cell expansion assay with overlapping peptide pools spanning the entire HCV genome Three patients with (near) normal CD4+ T cell counts (range 400-970 x 10(6)/L) either resolved (n=1) or temporary suppressed HCV RNA. In contrast, one patient with low CD4+ T cell counts (330 x 10(6)/L), had sustained high HCV RNA levels. All four patients had low HCV-specific CD8+ T cell responses, and similar magnitudes of CD4+ T cell responses. Interestingly, individuals with resolved infection or temporary suppression of HCV-RNA had HCV-specific CD4+ T cell responses predominantly against nonstructural (NS) proteins. While the individual with high HCV RNA plasma concentrations had CD4+ T cell responses predominantly directed against Core. Our data show that an acute HCV infection in an HIV-1 infected person can be suppressed in the presence of HCV-specific CD4+ T cell response targeting non-structural proteins. However further research is needed in a larger group of patients to evaluate the role of HIV-1 on HCV-specific T cell responses in relation to outcome of acute HCV infection.
Journal of Viral Hepatitis 03/2009; 16(4):239-48. DOI:10.1111/j.1365-2893.2009.01076.x · 3.91 Impact Factor
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