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Anti-hepatitis C Virus (anti-hepatitis + c_virus)

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Medical Sciences83%

Terms modified by Anti-hepatitis C Virus

  • anti-hepatitis c virus antibody
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    Selected Abstracts

    HCV796: A selective nonstructural protein 5B polymerase inhibitor with potent anti-hepatitis C virus activity In Vitro, in mice with chimeric human livers, and in humans infected with hepatitis C virus,

    HEPATOLOGY, Issue 3 2009
    Norman M. Kneteman
    Anti-hepatitis C virus (HCV) drug development has been challenged by a lack of experience with inhibitors inclusive of in vitro, animal model, and clinical study. This manuscript outlines activity and correlation across such a spectrum of models and into clinical trials with a novel selective nonstructural protein 5B (NS5B) polymerase inhibitor, HCV796. Enzyme assays yielded median inhibitory concentration (IC50) values of 0.01 to 0.14 ,M for genotype 1, with half maximal effective concentration (EC50s) of 5 nM and 9 nM against genotype 1a and 1b replicons. In the chimeric mouse model, a 2.02 ± 0.55 log reduction in HCV titer was seen with monotherapy, whereas a suboptimal dose of 30 mg/kg three times per day in combination with interferon demonstrated a 2.44 log reduction (P = 0.001 versus interferon alone) Clinical outcomes in combination with pegylated interferon and ribavirin have revealed additive efficacy in treatment naïve patients. Abnormal liver function test results were observed in 8% of HCV-796 patients treated for over 8 weeks, resulting in suspension of further trial activity. Conclusion: The RNA-dependent RNA polymerase inhibitor HCV796 demonstrated potent anti-HCV activity consistently through enzyme inhibition assays, subgenomic replicon, and chimeric mouse studies. Strong correlations of outcomes in the mouse model were seen with subsequent clinical trials, including a plateau in dose-related antiviral activity and additive impact from combination therapy with interferon. These outcomes demonstrate the utility of the range of in vitro and in vivo models now available for anti-HCV drug development and support the potential utility of polymerase inhibitors in future combination therapies for HCV treatment. (HEPATOLOGY 2009.) [source]

    Alcohol potentiates hepatitis C virus replicon expression

    HEPATOLOGY, Issue 1 2003
    Ting Zhang
    Alcohol consumption accelerates liver damage and diminishes the anti-hepatitis C virus (HCV) effect of interferon alfa (IFN-,) in patients with HCV infection. It is unknown, however, whether alcohol enhances HCV replication and promotes HCV disease progression. The availability of the HCV replicon containing hepatic cells has provided a unique opportunity to investigate the interaction between alcohol and HCV replicon expression. We determined whether alcohol enhances HCV RNA expression in the replicon containing hepatic cells. Alcohol, in a concentration-dependent fashion, significantly increased HCV replicon expression. Alcohol also compromised the anti-HCV effect of IFN-,. Investigation of the mechanism(s) responsible for the alcohol action on HCV replicon indicated that alcohol activated nuclear factor ,B (NF-,B) promoter. Caffeic acid phenethyl ester (CAPE), a specific inhibitor of the activation of NF-,B, abolished alcohol-induced HCV RNA expression. In addition, naltrexone, an opiate receptor antagonist, abrogated the enhancing effect of alcohol on HCV replicon expression. In conclusion, alcohol, probably through the activation of NF-,B and the endogenous opioid system, enhances HCV replicon expression and compromises the anti-HCV effect of IFN-,. Thus, alcohol may play an important role in vivo as a cofactor in HCV disease progression and compromise IFN-,-based therapy against HCV infection. [source]

    A study on sequence variations in pre-S/surface, X and enhancer II/core promoter/precore regions of occult hepatitis B virus in non-B, non-C hepatocellular carcinoma patients in Taiwan

    INTERNATIONAL JOURNAL OF CANCER, Issue 3 2009
    Chien-Hung Chen
    Abstract This study was to investigate the clinical significance and virologic factors of occult hepatitis B virus (HBV) infection in hepatocellular carcinoma (HCC) patients without hepatitis B surface antigen (HBsAg) or anti-hepatitis C virus (non-B, non-C) in Taiwan. Serum HBV DNA (occult HBV) was detected in 90 of 222 non-B, non-C HCC patients and 24 of 300 non-B, non-C controls without HCC. Of 90 occult HBV-infected HCC patients, the sequences of HBV pre-S/surface, X and enhancer II/core promoter/precore genes were analyzed from 40 patients. Direct sequencing of such genes was also performed in 24 non-B, non-C controls without HCC and 40 HBsAg-positive HCC controls. Compared with non-B, non-C controls without HCC, non-B, non-C subjects with HCC had significantly higher prevalence of occult HBV (p < 0.0001). Moreover, M1I and Q2K in pre-S2 gene and G1721A were more common in occult HBV-infected patients with HCC than in those without HCC. Compared with the HBsAg-positive HCC controls, occult HBV-infected HCC patients had higher frequencies of M1I and Q2K in pre-S2 gene, G185R and S210N in surface gene, A36T and A44L in X gene, and G1721A in enhancer II gene, and had lower rates of pre-S deletions and A1762T/G1764A, A1846T, G1896A and G1899A in core promoter/precore genes. Multivariate analysis showed Q2K in pre-S2 gene, G1721A and A1846T were independent factors for occult HBV-infected HCC. Our study suggested that the virological factors of HBV related to HCC were different between occult HBV-infected and HBsAg-positive patients. The G1721A, M1I and Q2K in pre-S2 gene may be useful viral markers for HCC in occult HBV carriers. © 2009 UICC [source]

    Antibody convergence along a common idiotypic axis in immunodeficiency virus and hepatitis C virus infections

    JOURNAL OF MEDICAL VIROLOGY, Issue 1 2002
    Michael D. GrantArticle first published online: 29 NOV 200
    Abstract The anti-idiotypic antibody 1F7 selectively binds antibodies against human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) gag, pol, and env proteins. We tested anti-hepatitis C virus (HCV) antibodies to investigate selection of the 1F7 idiotype on antibodies against other chronic pathogens. Twelve of 15 HCV-seropositive individuals co-infected with HIV had detectable antibodies against recombinant HCV core, 4 against HCV NS4 protein, and 3 against HCV NS3 protein. All four HCV-seropositive, non-HIV-infected individuals had antibodies against HCV core and NS4, while 3 had antibodies against NS3. The 1F7 idiotype was frequently present on antibodies against each of the HCV antigens in the HIV co-infected and non-HIV-infected groups. Antibodies against HCV, including antibodies recognizing the putative principal neutralizing determinant of HCV E2 protein, displayed skewed ,/, light chain usage consistent with clonal dominance. These observations extend the association between expression of the 1F7 idiotype and abnormal B cell clonal dominance in HIV and SIV infection to HCV infection and suggest that early establishment of an oligoclonal antibody response against HCV may freeze the B cell repertoire, impair adaptation to emergent HCV variants, and favor escape from neutralizing antibodies. We also demonstrated that expression of the 1F7 idiotype extends beyond antibodies against multiple antigens of AIDS-causing retroviruses to include antibodies against multiple antigens of an unrelated chronic hepatitis virus. Thus, distinct pathogens establishing chronic infection in the face of strong humoral immune responses select antibodies along a common idiotypic axis of the immune network. J. Med. Virol. 66:13,21, 2002. © 2002 Wiley-Liss, Inc. [source]

    Hepatitis C virus infection and oral lichen planus: a report from the Netherlands

    JOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 6 2000
    E. H. Meij
    Abstract: The reported frequency of anti-hepatitis C virus (HCV) antibodies in groups of cutaneous lichen planus (CLP) and/or oral lichen planus (OLP) patients varies from about 4% to 65%. Most of these studies have been performed in countries with a high overall prevalence of HCV infection in the general population, such as the southern European countries and Japan. Limited data are available from areas with a low prevalence of HCV infection. Therefore, we investigated the prevalence of HCV infection in a series of 55 patients with OLP in the Netherlands, which apparently has a low prevalence of HCV infection. None of the 55 patients revealed serological evidence of antibodies to HCV. The present data suggest that HCV infection in OLP patients in the Netherlands is probably not very common. A larger study group with a sex- and age-matched control group is required to advise against routine serological examination for HCV infection in Dutch OLP patients. [source]

    Changing aetiology of liver dysfunction in the new generation of a hepatitis B and C-endemic area: cross-sectional studies on adolescents born in the first 10 years after universal hepatitis B vaccination

    LIVER INTERNATIONAL, Issue 9 2008
    Jung-Ta Kao
    Abstract Background/Aim: Geographical variation in viral hepatitis infection complicates various levels of liver diseases. This study elucidates the changing aetiology of alanine transaminase elevation (ALT levels >40 IU/L) in a previously hepatitis-endemic township. Design/Methods: Five cross-sectional screenings were performed on teenagers born from 1984 to 1993. We examined hepatitis B surface antigen (HBsAg), anti-hepatitis C virus (anti-HCV), ALT and body mass index, and additionally checked hepatitis B envelope antigen (HBeAg) for positive HBsAg and HCV RNA for positive anti-HCV. Teenagers with ALT elevation underwent an ultrasonography examination. Results: This study enrolled 1788 (93.7%) of 1909 students, discovering individual prevalence of HBsAg (6.3%), anti-hepatitis B core (anti-HBc) (15.5%), anti-HCV (2.2%), overweight (22.4%), obesity (12.8%) and ALT >40 IU/L (3.7%). HBsAg and anti-HBc prevalence declined with trends, while obesity increased with trends (P<0.001). Among 66 ALT-elevated teenagers, prevalence percentages of risk factors were HBsAg (22.7%), anti-HCV (1.5%), obesity (45.5%), HBsAg with obesity (7.6%) and anti-HCV with obesity (3.0%). Additionally, obesity showed predominance (85.7%) among aetiologies of teenagers with fatty livers (60.9%). The independently associated factors of ALT elevation included being male (odds ratio, 2.18; 95% confidence interval, 1.21,3.93), HBsAg (4.25; 1.06,17.13), HBeAg (7.24; 1.64,31.9), HCV RNA (29.03; 5.8,145.29) and obesity (16.5; 8.79,30.98). Conclusion: In place of viral hepatitis, obesity is becoming the major aetiology of abnormal liver function among the young generation in a previously hepatitis-endemic area. [source]