Zeitspanne bis zur HCV-RNA „Negativierung“ bei Hepatitis C Virus (HCV) Typ 1-Infektion unter Peg-Interferon-alpha-2b plus Ribavirin-Therapie: Unterschiede in Abhängigkeit der Testsensitiviät (Indiv-1 Studiengruppe)

2007 ◽  
Vol 45 (08) ◽  
Author(s):  
T Berg ◽  
V Weich ◽  
G Teuber ◽  
H Klinker ◽  
B Möller ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Interferon Alpha ◽  
Hcv Rna ◽  
Interferon Alpha 2B

scholarly journals Hepatitis C Virus Clearance after Discontinuation of Pegylated Interferon Alpha-2a Monotherapy in a Child

2012 ◽  
Vol 2012 ◽  
pp. 1-4
Author(s):  
Takeshi Endo ◽  
Koichi Ito ◽  
Tokio Sugiura ◽  
Kenji Goto
Keyword(s):  
Hepatitis C Virus ◽  
Viral Load ◽  
Hepatitis C ◽  
Antiviral Therapy ◽  
Interferon Alpha ◽  
Antiviral Treatment ◽  
Pegylated Interferon ◽  
Hcv Rna ◽  
Pegylated Interferon Alpha ◽  
Present Patient

The present patient was a 4-year-old boy. His hepatitis C virus genotype was 2a, and his viral load was high (1400,000 U/mL). The pretreatment liver biopsy revealed no fibrosis or malignancy and mild chronic hepatitis; his Knodell's histological activity (HAI) score was 4. Single nucleotide polymorphism of IL28B (rs8099917) was major type. The patient began antiviral treatment with pegylated interferon alpha 2a (90 μg/week). At week 9, serum HCV RNA became undetectable, with a sensitivity of 50 copies/mL. Antiviral treatment was discontinued at week 11 because the ALT level increased to 610 U/L. After discontinuation of therapy, the patient’s serum HCV RNA status became positive again. The serum viral load increased to 100,000 U/mL. During this period, he had been observed without medication. Sixteen months after stopping treatment, serum HCV became undetectable. Over a 4-year period, HCV RNA became negative and his anti-HCV antibody titer gradually decreased. In conclusion, though antiviral therapy resulted in failure or incomplete therapy, a reduced viral load resulted in viral clearance in the present patient. Interleukin 28B genotype might have association with the clearance of hepatitis C virus after discontinuation of antiviral therapy.

scholarly journals Early Prediction of Nonresponders to Treatment with Interferon Alpha-2B and Ribavirin in Patients with Chronic Hepatitis C

2003 ◽  
Vol 17 (8) ◽  
pp. 483-487 ◽  
Author(s):  
Louis WC Liu ◽  
George Tomlinson ◽  
Tony Mazzulli ◽  
Alison Murray ◽  
Jenny Heathcote
Keyword(s):  
Chronic Hepatitis ◽  
Viral Load ◽  
Hepatitis C ◽  
Chronic Hepatitis C ◽  
Interferon Alpha ◽  
Baseline Viral Load ◽  
Hcv Rna ◽  
Interferon Alpha 2B ◽  
Quantitative Measurements ◽  
Treatment Responses

BACKGROUND: Treatment of chronic hepatitis C virus (HCV) infection with interferon alpha-2b and ribavirin is costly in terms of side effects, medical resources and drug costs. Furthermore, less than 50% of patients overall have a sustained virological response (SVR).OBJECTIVE: To determine if the log fall in HCV RNA between baseline and week 1 (b-wk1) and between baseline and week 4 (b-wk4) after starting treatment could identify the nonresponders.PATIENTS AND METHODS: Sixty-three patients who had completed a full course of therapy were identified. Quantitative measurements of HCV RNA were analyzed from stored sera, collected prospectively.RESULTS: SVR was achieved in 47.1% and 47.3% of patients in the b-wk1 and b-wk4 groups, respectively. No patients had an SVR with a fall in HCV RNA of less than 0.35 log10and 1.05 log10at week 1 and week 4, respectively. This accounted for 44.4% and 51.7% of the nonresponders in the b-wk1 and b-wk4 groups, respectively. Once the decline in viral load was known, genotype, age, sex and baseline viral load did not provide additional power in predicting treatment responses.CONCLUSION: A fall of 1.05 log10in HCV RNA at week 4 predicts those patients who will not respond, identifying one-half of all nonresponders; this allows therapy to be stopped early, without depriving any patient who would have an SVR from treatment.

Disappearance of Hepatitis C Virus RNA in Plasma during Interferon Alpha-2B Treatment in Hemophilia Patients

1992 ◽  
Vol 27 (3) ◽  
pp. 166-168 ◽  
Author(s):  
D. Bresters ◽  
E. P. Mauser-Bunschoten ◽  
H. T. M. Cuypers ◽  
P. N. Lelie ◽  
J. H. Han ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Interferon Alpha ◽  
Hepatitis C Virus Rna ◽  
Interferon Alpha 2B ◽  
Virus Rna

scholarly journals Characteristics of Hepatitis C Virus Infection in HIV-Infected People

2001 ◽  
Vol 12 (3) ◽  
pp. 157-163 ◽  
Author(s):  
Curtis L Cooper ◽  
Andrew D Badley ◽  
Jonathan B Angel
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Antiretroviral Therapy ◽  
Interferon Alpha ◽  
Highly Active Antiretroviral Therapy ◽  
Hcv Rna ◽  
Infected People ◽  
Highly Active ◽  
Interferon Alpha Therapy ◽  
History Of

Knowledge pertaining to hepatitis C virus (HCV)/human immunodeficiency virus (HIV) co-infection is currently incomplete or conflicting. Several points are well studied, however. Plasma HCV RNA levels are higher in matched HIV-infected people than in HIV-seronegative control subjects and are inversely correlated with CD4+T lymphocyte counts. HCV genotype does not appear to influence this value. Co-infected individuals develop histological and clinical features of HCV liver disease more rapidly than HIV-seronegative patients. Co-infected individuals appear to respond to interferon-alpha therapy equally as well as HIV-seronegative HCV-infected adults, but minimal information exists regarding the efficacy and toxicity of combination HCV therapy (interferon-alpha plus ribavirin) in this population. Adverse consequences of highly active antiretroviral therapy in co-infected patients include hepatic toxicity and, in a minority of patients, an 'immune restoration syndrome'. It is unclear whether long term, highly active antiretroviral therapy positively or negatively influences the natural history of HCV infection.

scholarly journals Inhibition of STAT Pathway Impairs Anti-Hepatitis C Virus Effect of Interferon Alpha

2016 ◽  
Vol 40 (1-2) ◽  
pp. 77-90 ◽  
Author(s):  
Lan-Juan Zhao ◽  
Sheng-Fei He ◽  
Yuan Liu ◽  
Ping Zhao ◽  
Zhong-Qi Bian ◽  
...  
Keyword(s):  
Gene Expression ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Interferon Alpha ◽  
Hcv Infection ◽  
Hcv Rna ◽  
Jak Inhibitor ◽  
Stat Signaling ◽  
Antiviral Gene ◽  
Stat Pathway

Background/Aims: Signal transducer and activator of transcription (STAT) pathway plays an important role in antiviral efficacy of interferon alpha (IFN-α). IFN-α is the main therapeutic against hepatitis C virus (HCV) infection. We explored effects of IFN-α on HCV replication and antiviral gene expression by targeting STAT. Methods: In response to IFN-α, STAT status, HCV replication, and antiviral gene expression were analyzed in human hepatoma Huh7.5.1 cells before and after cell culture-derived HCV infection. Results: IFN-α treatment induced expression and phosphorylation of STAT1 and STAT2 in Huh7.5.1 cells. Pretreatment of Huh7.5.1 cells with a mAb to IFN alpha receptor (IFNAR) 2 decreased IFN-α-dependent phosphorylation of STAT1 and STAT2, whereas pretreatment with an IFNAR1 mAb increased such phosphorylation, suggesting that IFNAR mediates IFN-α-triggered STAT signaling. During HCV infection, STAT1 and STAT2 phosphorylation could be rescued by IFN-α and IFN-α-induced phosphorylation of STAT1 and STAT2 was impaired. Inhibition of STAT pathway by Jak inhibitor I significantly enhanced HCV RNA replication and viral protein expression. Antiviral genes coding for IFN regulatory factor 9 and IFN-stimulated gene 15 were up-regulated by IFN-α during HCV infection but such up-regulation was abrogated by Jak inhibitor I. Conclusion: These results establish that activation of STAT pathway is essential for anti-HCV efficacy of IFN-α. Impairment of IFN-α-triggered STAT signaling by HCV may account for evading IFN-α response.

Sign in / Sign up

Export Citation Format

Share Document