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  • The HCV Ag immunoassay has been shown from previous studies

    2021-11-22

    The HCV-Ag immunoassay has been shown from previous studies to be an adequate alternative to the two-stage diagnostic process [6], [9], [16]. Kesli et al. reported a high correlation coefficient of 0.864 when comparing HCV core antigen levels with HCV RNA levels (detected using Qiagen HCV RNA test; Qiagen, Hilden, Germany) [17]. Similar results were reported by various other studies. One study conducted in a township in southern Taiwan by Kuo et al. compared HCV RNA levels with HCV-Ag and anti-HCV signal-to-cutoff ratios in 405 subjects [18]. With HCV RNA detected at >15 IU/ml and HCV-Ag considered reactive at ≥3 fmol/L, Kuo et al. found significant linear regressive correlation between HCV RNA levels and HCV-Ag, with 97.8% sensitivity and 97.1% specificity. Another study conducted by Mederacke et al. found good correlation between HCV RNA levels and HCV-Ag levels with correlation coefficient of 0.75, determined also through Roche TaqMan PCR and Abbott ARCHITECT HCV-Ag assay, respectively [9]; while Wang et al. also found a high correlation coefficient of 0.891, using enzyme-linked immunosorbent assay (ELISA) for detection of HCV-Ag and Abbott RealTime platform (Abbott Molecular Inc., Des Plaines, IL) for HCV RNA levels [19]. In our study, the HCV-Ag immunoassay detected the various genotypes of HCV with a predominance of Fluorescein-12-dUTP sale 1 and 2, corresponding to the genotypic distribution of HCV in the Asia-Pacific region [11]. Specifically, there was stronger correlation between HCV RNA titers and HCV-Ag immunoassay in genotype 1 (r = 0.945) compared with genotype 2 (r = 0.862). In contrast, in studies by Mederacke et al. and Durante-Mangoni et al. [9], [13], both showed stronger correlation of genotype 2 (r = 0.77 and r = 0.65 respectively) with HCV molecular assay than genotype 1 (r = 0.72 and r = 0.53 respectively). Of note, the correlation coefficients of both genotype 1 and genotype 2 in both of these studies are considerably lower than our study, indicating there remains inconsistency amongst studies in the efficacy of HCV-Ag immunoassays in genotyping HCV RNA positive patients. Possible explanations for this discordance can include variable quality of stored sera, and a meta-analysis will be useful in investigating factors affecting efficacy of HCV-Ag immunoassays.
    Acknowledgement This study was supported by a grant from Chang Gung Memorial Hospital and was funded by Abbott Diagnostics for providing reagents.
    Introduction Hepatitis C virus (HCV) infection is frequently associated with several extrahepatic disorders [1]. Among them, mixed cryoglobulinaemia (MC) is detected in 40–60% of HCV patients. Only 5–10% of these patients are symptomatic [1]. Four recent cohort studies and a meta-analysis evaluated only in HCV-monoinfected patients the benefit of direct-acting antivirals (DAA) on cryoglobulin levels as well as MC-related symptom manifestation [2], [3], [4], [5], [6]. Among HIV-HCV-coinfected patients, it is thought that HIV infection may alter the clinical course and impact the cryoglobulin clearance rate during HCV antiviral treatment [7]. However, no study to date has investigated the impact of DAA on MC in HIV-HCV-coinfected patients. Therefore, we investigated the evolution of cryoglobulin levels in HIV-HCV-coinfected MC patients in comparison with HCV-monoinfected MC patients following DAA administration.
    Materials and methods
    Results
    Discussion Such results were previously reported but only in HCV-monoinfected patients [2], [3], [4], [5]. Viral eradication is to date the best strategy to prevent further production of cryoglobulins, which are directly involved in MC pathogenesis. As suggested by others, despite viral clearance, the underlying MC pathogenetic process could persist because of active lymphoproliferative disorders, auto-immunity, or cancers [9], [10]. As previously reported, HIV-HCV patients rarely have symptoms associated with circulating cryoglobulins [7], [11]. Here, only one out of 12 patients had symptomatic MC. Absence of symptoms in HIV-HCV-coinfected patients may be explained by the cell-mediated immune defect associated with HIV infection. Our results also suggest a trend for a lower cryoglobulin level among the HIV-HCV population compared with HCV-monoinfected patients. A higher CD4 cell count level has also been associated with a higher level of circulating cryoglobulins in HIV-HCV patients [11], [12]. Moreover, MC-associated symptoms may be revealed after immune restoration during active cART [11]. This supports an independent role of HIV explaining that a weak immune reconstitution or absence of active cART may favour the absence of MC as found in the HIV-HCV population [12] or in HIV-monoinfected patients [13].