Acute Hepatitis C in HIV-1 Infected Japanese Cohort: Single Center Retrospective Cohort Study (original) (raw)
Related papers
The Journal of Infectious Diseases, 2005
Objective. To assess hepatitis C virus (HCV) antibody prevalence in the EuroSIDA cohort, along with survival, human immunodeficiency virus (HIV)-1 disease progression, virologic response (plasma HIV-1 RNA load of !500 copies/mL), and CD4 cell count recovery by HCV serostatus in patients initiating highly active antiretroviral therapy (HAART). Results. HCV serostatus at or before enrollment was available for 5957 patients; 1960 (33%) and 3997 (67%) were HCV seropositive and seronegative, respectively. No association between an increased incidence of acquired immunodeficiency syndrome-defining illnesses or death and HCV serostatus was seen after adjustment for other prognostic risk factors known at baseline (adjusted incidence rate ratio [IRR], 0.97 [95% confidence interval {CI}, 0.81-1.16]). However, there was a large increase in the incidence of liver disease-related deaths in HCV-seropositive patients in adjusted models (IRR, 11.71 [95% CI, 6.42-21.34]). Among 2260 patients of known HCV serostatus initiating HAART, after adjustment, there was no significant difference between HCV-seropositive and-seronegative patients with respect to virologic response (relative hazard [RH], 1.13 [95% CI, 0.84-1.51]) and immunologic response, whether measured as a у50% increase (RH, 0.94 [95% CI, 0.77-1.16]) or a у50 cells/mL increase (RH, 0.92 [95% CI, 0.77-1.11]) in CD4 cell count after HAART initiation. Conclusions. HCV serostatus did not affect the risk of HIV-1 disease progression, but the risk of liver diseaserelated deaths was markedly increased in HCV-seropositive patients. The overall virologic and immunologic responses to HAART were not affected by HCV serostatus. Hepatitis C virus (HCV) coinfection has become one of the most challenging clinical situations to manage in HIV-1-infected individuals. Indeed, at present, endstage liver disease is the cause of 17%-45% of in-hospital deaths in HIV-1-infected individuals in the West [1-3]. Because of shared routes of transmission, an estimated 30% of HIV-1-infected individuals are coin
Factors Associated with Seronegative Chronic Hepatitis C Virus Infection in HIV Infection
Clinical Infectious Diseases, 2007
antibody (anti-HCV) negative, but HCV RNA positivity occurs in individuals infected with human immunodeficiency virus (HIV). However, associated factors are not well established because of the small number of reported cases. ) determined factors associated with HCV RNA positivity in anti-HCV-negative subjects. HCV enzyme immunoassay 2.0 was used to determine anti-HCV status.
BMC Infectious Diseases, 2014
Background: HIV infection leads to a faster progression of liver disease in subjects infected with HCV, as compared with HCV mono-infected patients. Previous reports suggest that sustained virological response (SVR) rates are lower in HIV/HCV coinfection than in HCV monoinfection. We aimed to compare SVR rates of these two populations. Methods: We retrospectively analyzed clinical, biochemical and virological data of HCV and HIV/HCV infected patients with HCV genotypes 2 and 3 who started anti-HCV treatment between March 2004 and November 2012, at a single large center. Intention-to-treat (ITT) and per-protocol (PP) analysis were performed. Univariate and multivariate logistic regression analyses were performed to assess predictors of SVR. Results: 461 patients were analyzed: 307 (66.6%) males, 76 (16.5%) infected with HIV. Several differences at baseline between HCV monoinfected and HIV/HCV coinfected patients were observed. HCV monoinfected group was characterized by higher prevalence of genotype 2 (53% vs 5.3%), higher baseline HCV viral load (50% vs 35%), shorter mean duration of treatment (19 vs 41 weeks), more frequent use of peginterferon alfa-2a (84.5% vs 69.7%), lower prevalence of cirrhosis (6% vs 31.6%). Globally, SVR was achieved by 353 (76.6%) patients and 321 (83.8%) in the PP analysis. No statistically relevant differences were found in SVR rates between the two groups, either in ITT [78.2% (n = 301/385) vs 68.4% (n = 52/76), p =0.066, respectively] than in PP analysis [83.6% (n = 276/330) vs 84.9% (n = 45/53), p = 0.8]. ITT analysis: At univariate and multivariate analysis, baseline HCV-RNA >500.000 IU/ml [OR 0.4 (0.24-0.66), p = 0.0004], use of peginterferon alfa-2b [OR 0.5 (0.27-0.93) p = 0.033], platelets count <130.000/mm 3 [OR 0.45 (0.2-0.99), p = 0.045], interruption of peginterferon therapy [OR 0.2 (0.1-0.4), p<0.0001], interruption of ribavirin treatment [OR 0.34 (0.17-0.69), p = 0.0026] were related with lower rate of SVR. PP analysis: Only HCV-RNA >500.000 IU/ml and interruption of ribavirin were related to lower probability to achieve SVR at both univariate and multivariate analysis [OR 0.41 (0.23-0.75), p = 0.004; OR 0.24 (0.1-0.5), p = 0.0004, respectively]. Conclusions: Higher baseline viral loads and interruption of peginterferon and/or ribavirin were associated with a poor outcome of anti-HCV treatment while HIV infection was not related to major or minor probability to achieve SVR.
Pathogens and Global Health, 2016
Background: Human immunodeficiency virus (HIV)/hepatitis C virus (HCV) coinfection has become a serious public health problem. The influence of HIV/HCV coinfection on plasma HCV RNA loads and clinical criteria which are usually regarded as a predictor of the progress of liver disease have not been reliably evaluated. Objectives: This study investigated the impact of HIV infection on HCV RNA load and clinical indexes in Yazd and Tehran. Materials and methods: HCV/HIV-coinfected patients and HCV-monoinfected controls were examined and compared for plasma HCV RNA and related risk factors such as HCV genotypes, liver enzymes, and transmission routes. Results: A total of 54 HCV/HIV-coinfected patients and 88 HCV-monoinfected controls were studied. The HCV RNA load mean was significantly higher in HCV/HIV-coinfected patients than in HCV-monoinfected patients (p < 0.001). HCV RNA load mean in patients infected with HCV without anti-HCV therapy was lower than HIV/ HCV patients with and without highly active antiretroviral therapy that this difference was significant (p < 0.001). The HCV RNA levels were significantly higher in HIV/HCV genotype 3a coinfected patients than in genotype 3a monoinfected patients (p < 0.001). HIV RNA levels were lower in genotype 1a infected patients than in genotype 3a infected patients, but this difference was not significant statistically. The ALT mean levels were significantly higher in genotype 3a HIV/HCV-coinfected patients than in genotype 3a HCV-monoinfected patients (p < 0.001). Conclusions: HIV/HCV coinfection leads to a significant increase in plasma HCV RNA. Further evaluations of the effects of ART and HIV infection on the course of HCV infection and the response to treatment against HCV infection in other and different genotypes are also needed. Moreover, HIV-infected patients should be screened regularly for HCV coinfection, particularly if they are in high-risk groups such as IDUs and recipients of blood transfusions.
High rate of seronegative HCV infection in HIV‑positive patients
Biomedical Reports, 2013
Co-infection with human immunodeficiency virus (HIV) and hepatitis C virus (HCV) is a significant global health problem. The two viruses are transmitted with high efficacy via blood-to-blood contact, mainly intravenous drug use (IVDU), whereas HCV is less easily transmitted sexually. Antibody testing is the main screening method for HCV infection, although it may not be the optimal option for HIV infection. The aim of this study was to investigate HCV infection in HIV-positive patients, with and without a detectable anti-HCV antibody response. A total of 187 plasma samples were obtained from HIV-positive patients in Surabaya, Indonesia and examined for anti-HCV [HCV enzyme immunoassay (EIA) 3.0], HCV genotype̸subtype [reverse transcription-polymerase chain reaction (RT-PCR) using primers targeting a part of NS5B/5'UTR followed by sequencing] and HCV viral load (quantitative RT-PCR). A total of 119 patients (63.6%) were found to be anti-HCV-positive and, among these, HCV RNA was detected in 73 (61.3%), with HCV-1a as the predominant subtype (31.5%). Of the 68 anti-HCV-negative samples, HCV RNA was detected in 26/68 (38.2%) mostly as the HCV-3a subtype (50%). High HCV viral loads were more common among the HCV-seropositive patients. The HCV-seropositive samples with detected HCV RNA were mostly obtained from HIV-positive patients with parenteral transmission (IVDU) (76.7%); however, the HCV-seronegative samples with detected HCV RNA were mostly from patients who had acquired HCV through heterosexual transmission (61.5%). In conclusion, HIV-positive patients were at high risk of becoming co-infected with HCV and several remained HCV-seronegative. Furthermore, there may exist differences in HCV seropositivity and subtypes between HIV-positive patients who acquired HCV sexually and those who acquired HCV parenterally.
The new microbiologica, 2015
Single nucleotide polymorphisms (SNPs) rs12979860 and rs8099917 near the interleukin 28B gene are predictors of virological response (SVR) to IFN-based therapy for monoinfected chronic hepatitis C patients. We retrospectively evaluated the impact of IL28B SNPs and other factors on SVR in a cohort of 102 HIV-1/HCV-coinfected patients treated with pegylated interferon-? (peg-INF?) and ribavirin. Data on baseline features and virological response at different time-points were collected. Overall, 89/102 patients (87%) were males, 44 (43%) of whom infected with HCV genotype 1; SVR was achieved by 50 patients (49%). A univariate logistic regression analysis demonstrated that rs129679860 SNP genotype CC (p<0.034), rs8099917 SNP genotype TT (p<0.01), HCV genotype 2 or 3 (p<0.0001), low HCV viral load (p<0.028) and RVR (rapid virological response) (p<0.0001) were associated with a higher likelihood of SVR. Multivariate analysis confirmed only RVR and HCV genotype as independen...
Longitudinal study in HIV/HCV-coinfected HAART-naive patients and role of HCV genotype
Journal of Clinical Virology, 2005
To evaluate the impact of highly active antiretroviral therapy (HAART) on the course of hepatitis C (HCV) infection, we studied the biological and virological characteristics of 23 HCV/HIV-coinfected HAART-naive patients. The HCV genotype, HCV and HIV viral loads, serum alanine aminotransferase, CD4 + and CD8 + cell/mm 3 were determined at baseline, 1 month, 6 months and 12 months after initiation of HAART. Results were analyzed both in terms of total population and of HCV genotype. The study of the total population suggests that this therapy did not determine a significant alteration of HCV viremia and levels of ALT, while a significant decrease in HIV viremia (−1.7 log 10 at one year from the start of HAART) and increase in CD4 + counts was observed (P < 0.005). The biological and virological parameters of HCV/HIV coinfection differed according to the HCV genotype. In particular, only genotype 4 showed a significant inverse correlation between HCV and HIV viral loads.
Scientific Reports, 2015
Data are limited on the effectiveness and safety of peginterferon plus ribavirin in HIV-infected Asian patients with acute or chronic HCV infection. HIV-infected Taiwanese patients with acute HCV infection received peginterferon plus weight-based ribavirin for 24 weeks (n = 24) and those with chronic HCV genotype 1 or 6 (HCV-1/6) and HCV genotype 2 or 3 (HCV-2/3) infection received response-guided therapy for 12–72 and 24–48 weeks, respectively (n = 92). The primary endpoint was sustained virologic response (SVR), defined as undetectable HCV RNA 24 weeks off-therapy. The SVR rates were 83% and 72% in patients with acute and chronic HCV infection (p = 0.30) and 68% and 72% in patients with chronic HCV-1/6 and HCV-2/3 infection (p = 0.48), respectively. While no factors predicted SVR in acute HCV and chronic HCV-2/3 infection, age (odds ratio [OR] per 1-year increase: 0.88, 95% confidence interval [CI]: 0.78–0.99, p = 0.04), HCV RNA (OR per 1-log10 increase: 0.18, 95% CI: 0.03–0.98, p...
Journal of Viral Hepatitis, 2006
Summary. To evaluate, among 70 hepatitis C virus (HCV)-monoinfected and 36 human immunodeficiency virus (HIV)-coinfected naïve patients with genotypes 1/4 receiving weight-adjusted pegylated interferon-α-2b/ribavirin, viral kinetics and the feasibility to predict treatment failure measuring early HCV-RNA decreases. HCV-RNA was assessed at baseline, weeks 4, 12 and 24. Receiver operating characteristic (ROC) curves were calculated to determine the most sensitive cut-off values of viral decrease at week 4 predicting treatment failure. Baseline predictors of failure were evaluated by univariate and multivariate analyses. Despite similar baseline HCV-RNA (5·75 vs 5·72 log10IU/ml, P = 0·6), HCV monoinfection led to significantly lower HCV-RNA values at weeks 4 (3·7 vs 4·3 log10IU/ml, P = 0·01), 12 (2·3 vs 3·5 log10IU/ml, P = 0·01) and 24 (1·4 vs 3·3 log10IU/ml, P = 0·001) and a higher rates of viral clearance at weeks 24 (60%vs 36%, P = 0·02), 48 (46%vs 25%, P = 0.03) and 72 (37%vs 17%). The lack of achieving an HCV-RNA decrease of at least 1 log10 at week 4 was highly predictive of treatment failure for HCV-monoinfected patients (Se 100%, Sp 50%, positive predictive value (PPV) 57%, negative predictive value (NPV) 100%, ROC curve area, 0·86 [95% confidence interval (CI) 0·77–0·95], but not for HCV/HIV-coinfected patients (cut-off, 0 log10, Se 100%, Sp 27%, PPV 21%, NPV 100%, ROC curve area, 0·71 (95% CI 0·49–0·93). HIV coinfection was independently associated with failure (odds ratio 2.95, 95% CI 1·08–8.04, P = 0·01). Thus the magnitude of HCV-RNA decreases at week 4 correlated with treatment response. Significant differences in viral kinetics and cut-off values predicting nonresponse suggest a slower HCV clearance rate in HIV coinfection, which was independently associated with treatment failure.