A study of innate and adaptive immune responses in beta-thalassemic patients with chronic hepatitis C virus infection.

Thalassemia major is an inherited disorder particularly common in people of Mediterranean, African, and Southeast Asian ancestry. Hepatitis C virus (HCV) is responsible for 80 - 90% of post transfusion hepatitis in beta-Thalassemic patients. Marked liver iron overload, which is often inevitable in patients on regular blood transfusion, and HCV infection have been shown to have a potentiating effect on hepatic fibrogenesis in thalassemic patients. This study aimed at investigating the impact of combined chronic hepatitis C and beta-Thalassemia on innate and adaptive immune responses. The study was conducted on 60 patients and 15 apparently healthy controls. Patients were dived into three groups: group 1: 35 patients with combined beta-thalassemia and chronic hepatitis C (CHC) (betaTH/CHC), group II: 15 beta-thalassemia patients without HCV infection (betaTH), group III: 10 patients with chronic hepatitis C infection (CHC). Assessment of the number of CD3+, CD4+, CD8+ T cells, NK cells, and NKT cells was done by flowcytometry. Human IFN-delta and IL-15 levels were estimated by Enzyme -Linked Immunosorbent Assay (ELISA). betaTH/CHC patients had significantly reduced numbers of conventional T lymphocytes, NK, NKT, CD4+, and CD8+ T cells when compared to betaTH patients. Serum IFN-gamma levels were significantly reduced in betaTH/CHC patients (2.57 pg/ml) in comparison to CHC patients (6.89pg/ml) and normal controls (4.73 pg/ml). A significant elevation of serum IL-15 levels in betaTH/CHC patients (38.04pg/ml) was found when compared to betaTH patients (16.22 pg/ml). Splenectomized patients showed reduced numbers of NK cells, NK T cells and lower CD4:CD8 ratio in comparison to non-splenectomized ones among betaTH/CHC patients. In conclusion our data show an obvious defective cellular innate immunity (NK & NKT cells) and cellular adaptive immunity (CD4+ T cells, CD8+ T cells, & INF-gamma) in (betaTH/CHC) patients, in comparison to (betaTH) patients. This observation suggests a potentiating effect of both CHC and beta-thalassemia on depression of innate and adaptive immune status in these patients