Evaluation of the HCV core antigen assay as a second-line supplemental test for diagnosis of active hepatitis c infection

Hepatitis C virus core [HCV] antigen assays have been produced to exclude infectious donations collected the preseroconversion window phase. For the same purpose, we evaluated the specificity and sensitivity of a novel hepatitis C virus core antigen detection immunoassay and the applications of this assay in clinical diagnosis. Samples were collected from 30 anti-HCV antibody negative healthy subjects [Gi], and 46 anti-HCV antibody positive patients [G2]. All included samples were subjected to HCV core antigen and HCV-RNA PCR. Among the 46 anti-HCV Ab positive samples, HCV core antigen was positive in 38 samples from 40 samples positive for HCV-RNA with sensitivity of 95% [38/40]. All the 30 anti-HCV Ab negative samples [n=30] were negative for both HCV core antigen and HCV-RNA with specificity of 100% .There was no significant variation in the sensitivity of HCV core antigen between genotype 1 [100%] and genotype 4 [94.5%]. Viral load in HCV core antigen positive samples [906653 +/- 133803] was significantly increased than that of HCV core antigen negative samples [16342 +/- 5245] with P value<0.05. HCV core antigen assay is a useful method in screening strategy of HCV infection and provides a reliable means of distinguishing between current and cleared HCV infections that is well correlated with HCV-RNA testing

HCV genotype and "Silent" HBV coinfection: two main risk factors for a more severe liver disease

To evaluate whether HCV genotype and "silent" HBV infection may be related to a more severe clinical presentation of liver disease. 40 anti-HCV/HCV-RNA positive, HB5Ag/anti-HB5 negative patients with chronic hepatitis [27 males and 13 females, median age 43 +/- 6.98] years, were studied on presentation at National Liver Institute, Menofia University. Presence of serum anti-HBc, in absence of HBsAg and anti-HBs, was considered a marker of "silent" HBV infection. Two main diagnosis groups were established: the mild liver disease group [G1 n20], and the severe liver disease group [G2 n20]. The prevalence of silent HBV infection in HCV patients was 50% where out of the 40 anti-HCV/HCV-RNA positive, HBsAg and anti-HBs negative patients with a definite diagnosis, 20 patients [50%] were anti-HBc positive. Of the 20 anti-HBc positive patients, HBeAg/anti-HBc system was investigated, where 14 patients [70%] were anti-HBe positive and 6 patients [30%] were anti-HBe negative. None of these 20 patients was HBeAg positive. Twelve [60%] out of the 20 HBcAb ve cases were found to be positive for serum HBV-DNA by PCR. In the present study, it was found that the prevalence of a severe liver disease was higher in anti-HBc positive cirrhotic HCV patients lacking both HBsAg and anti-HBs [silent HBV infection] than in cirrhotic HCV patients with no markers of HBV infection [80% vs. 20%, P<0.001], indicating that a "silent HBV infection" may unfavorably influence the course of the disease. This was observed both in HBV-DNA positive and in HBV-DNA negative patients and regardless HCV genotype. Silent HBV infection seems to be a major risk factor for an unfavorable course of the disease. The observation that anti-HBc positive/HBV-DNA negative patients show a similar prevalence of severe liver disease to anti-HBc/HB V-DNA positive patients and a significantly higher prevalence than anti-HBc negative cases supports further the view that isolated serum anti-HBc is a marker of clinical significance