[show abstract][hide abstract] ABSTRACT: Enhanced replication of hepatitis C virus (HCV) is well described in the setting of moderate to severe immunosuppression. The aims of this retrospective study were to determine the incidence of enhanced HCV replication in hepatocellular carcinoma (HCC) patients undergoing transarterial chemolipiodolization (TACL) and to identify the factors associated with enhanced replication of HCV. The clinical pattern of enhanced HCV replication was compared with hepatitis B virus (HBV) reactivation during TACL.
This study enrolled 49 anti-HCV-seropositive patients who were diagnosed with HCC between January 2005 and December 2010 and who underwent TACL using epirubicin and/or cisplatin with consecutive HCV RNA copies checked. For comparison, 46 hepatitis B surface antigen(1)-positive patients with HCC who were treated with TACL were also enrolled. The frequency, associated factors, and clinical outcomes of enhanced HCV replication were analyzed and compared with those of HBV reactivation during TACL.
Enhanced replication of HCV occurred in 13 (26.5%) of the 49 anti-HCV-seropositive patients during TACL. Of these 13 patients, 4 developed hepatitis, but none of the subjects developed decompensation due to the hepatitis. No significant clinical factors for enhanced HCV replication during TACL were found. Compared with HBV reactivation, the frequency of hepatitis attributed to enhanced HCV replication was significantly lower than that for HBV reactivation (8.2% vs. 23.9%, P=0.036).
TACL can enhance HCV replication; however, the likelihood of hepatitis and decompensation stemming from enhanced HCV replication was lower than that for HBV reactivation in patients undergoing TACL.
The Korean journal of hepatology. 12/2011; 17(4):299-306.
[show abstract][hide abstract] ABSTRACT: The virologic determinants of progressive liver disease associated with hepatitis B virus (HBV) remain unclear. Previous investigations have associated HBV disease with specific mutations but this association may be confounded by HBV genotype, HLA haplotype of the infected individual or both. The association between non-synonymous mutations located within putative cytotoxic T-lymphocyte directed epitopes (CDE) of the HBV core region and disease states was investigated. Subjects infected with HBV were enrolled from a clinical cohort in Seoul, Korea, and HBV core gene sequences were analyzed for mutational patterns inside and outside of CDE with respect to subject demographics and HBV-related disease states. No specific mutation or pattern of mutations were associated with progressive disease states; however, individuals with cirrhosis and hepatocellular carcinoma had greater numbers of non-synonymous mutations within CDE when compared to those with chronic HBV infection who were HBeAg positive (P = 0.007 and 0.026, respectively). In conclusion, this study demonstrates that HBV disease progression is associated with viral escape mutations that are a marker of CTL activity. These data suggest that the number of non-synonymous mutations in the HBV core region may predict HBV disease progression better than any single mutation or pattern of mutations.
Journal of Medical Virology 12/2011; 83(12):2082-7. · 2.37 Impact Factor
[show abstract][hide abstract] ABSTRACT: Natural killer (NK) cells play an important role in innate immunity, especially in the response to viral infections, such as hepatitis C virus (HCV). Killer cell immunoglobulin-like receptors (KIRs) are the primary receptors of NK cells that mediate innate immunity. KIRs are also involved in acquired immunity, because some KIRs are expressed on the surface of certain subsets of T cells. In this study, the frequency of KIR genes, HLA-C allotypes, and combinations of KIR genes with their HLA-C ligands were evaluated in two different groups of the Korean population: controls and patients with chronic HCV infection. The study population consisted of 147 Korean patients with chronic HCV infection. The frequency of KIR2DS2 in patients with chronic HCV infection was 9.5% which was significantly lower than 19.5% of the control (P < 0.01). However, there were no significant differences in the frequency of other KIR genes, HLA-C allotypes or different combinations of KIR genes with their HLA-C ligands. This study can contribute to the further prospective study with a larger scale, suggesting the assumption that KIR2DS2 might aid in HCV clearance by enhancing both the innate and acquired immune responses of people in Korea.
Journal of Korean medical science 11/2011; 26(11):1483-8. · 0.84 Impact Factor
[show abstract][hide abstract] ABSTRACT: CD133 is a cancer stem-cell (CSC) marker associated with radioresistance and chemoresistance in various cancers. In the present study, CD133-expressing liver cancer cells following radiation exposure showed higher activation of MAPK/PI3K signaling pathway and reduction in reactive oxygen species levels compared to CD133- cells. The in vivo study with a xenograft model showed increased tumor formation in irradiated CD133+ cell-injected nude mice compared to the CD133- group, suggesting that CD133 contributes to radioresistance in HCC. Therefore, CD133-expressing liver cancer cells have anti-apoptotic and radioresistance properties that may be useful to improve anti-cancer treatments, including chemotherapy/radiotherapy of HCC.
Cancer letters 10/2011; 315(2):129-37. · 4.86 Impact Factor