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.
Different core-specific T cell subsets are expanded in chronic hepatitis C with advanced liver disease
CYTOKINE
Authors: Cachem, Fabio C. O. F.; Dias, Aleida S.; Monteiro, Clarice; Fernandes, Gabriel; Delphim, Leticia; Tavares, Felipe; Maciel, Alessandra M. A.; Amendola-Pires, Marcia M.; Brandao-Mello, Carlos Eduardo; Andrade, Regis Mariano; Bento, Cleonice A. M.
Abstract
Chronic hepatitis C (CHC) is frequently related to liver fibrosis, and several studies have suggested that the immunological activity of HCV antigens contributes to hepatic damage. In the present study, among structural and non-structural HCV antigens, elevatedIL-1 beta, IL-6, IL-17 levels were secreted by PBMC cultures obtained from CHC patients following stimulation with core antigen. Moreover, the percentage of core-specific IL-6(+)IL-17(+) (CD4(+) and CD8(+)) T cells was significantly higher in patients with worsehepatic lesions, determined on the Metavir scale. When compared with healthy subjects, the percentage of circulating Treg cells was elevated in CHC patients, mainly among those with advanced liver fibrosis. Nevertheless, in this last group of patients, the proportion of CD39(+) Treg subsets was very low. Finally, the percentage of senescent (CD57(+) CD28(-)) and exhausted (PD-1(+) CD28(+)) core-specific T cells in CHC patients was also found to be a result of fibrotic hepatic status. In summary, imbalances between different core-specific T cell subsets are associated with liver fibrosis severity.