Nanomedicine as a future therapeutic approach for Hepatitis C virus
NANOMEDICINE
Authors: Abd Ellah, Noura H.; Tawfeek, Hesham M.; John, James; Hetta, Helal F.
Abstract
Hepatitis C virus (HCV) is not easily cleared from thehuman body and in most cases turned into chronic infection. This chronicity is a major cause of liver damage, cirrhosis and hepatocellular carcinoma. Therefore, immediate detection and treatment of HCV guarantees eradication of the virus and prevention of chronicity complications. Since discovery of HCV in 1989, several emerging treatments were developed such aspolyethylene glycol(PEG)-ylated interferon/ribavirin, direct acting antivirals and host targeting antivirals. Despite the progress in anti-HCV therapy, there is still a pressing need of new approaches for affordable and effective drug delivery systems using nanomedicine. In this review, the contribution of nanoparticles as a promising delivery system for HCV immunizing, diagnostic and therapeutic agents are discussed.
Hepatitis B and hepatitis C viral infections in patients with chronic lymphocytic leukemia
CANADIAN JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
Authors: Minuk, Gerald Y.; Lerner, Betty; Gibson, Spencer B.; Johnston, James B.; Uhanova, Julia; Andonov, Anton; Wu, Jun
Abstract
Background: Whether chronic hepatitis B virus (HBV) or hepatitis C virus (HCV) infections contribute to the pathogenesis and/or course of chronic lymphocytic leukemia is unclear. Objective: To document the prevalences of HBV and HCV infections in chronic lymphocytic leukemia patients, and to determine whether infected patients experience more aggressive disease than those without infection. Methods: Patient sera were screened for antibodies to HBV core antigen and HCV (anti-HCV) using ELISA; both sera and peripheral blood lymphocytes were further tested (regardless of antibody results) for HBV-DNA and HCV-RNA using real-time polymerase chain reaction. Prognostic markers for chronic lymphocytic leukemia included Rai stage, IgVH mutational status, beta(2)-microglobulin levels, Zap-70 and CD38 status. Results: Fourteen of 222 (6.3%) chronic lymphocytic leukemia patients and two of 72 (2.8%) healthy controls tested positive for previous or ongoing HBV infection (OR 2.4 [95% CI 0.5 to 7.7]; P-0.25) while four of 222 (1.8%) chronic lymphocytic leukemia patients and one of 72 (1.4%) controls tested positive for HCV markers (OR 1.3 [95% CI 0.2 to 6.4]; P=0.81). The levels and distribution of the various indicators of aggressive chronic lymphocytic leukemia disease were similar among HBV- and HCV- infected and uninfected patients. Survival times were also similar. Occult HBV and HCV infection (HBV-DNA or HCV-RNA positive in the absence of diagnostic serological markers) were uncommon in chronic lymphocytic leukemia patients (0.5% and 1.8%, respectively). Conclusions: The results of the present study do not support the hypothesis that HBV or HCV infections play an important role in the pathogenesis or course of chronic lymphocytic leukemia.