Interleukin-28B Polymorphisms Predict the Efficacy of Peginterferon Alpha in Patients With Chronic Hepatitis B: A Meta-Analysis

Background: Polyethylene glycol interferon alpha (PEG-IFN-α) is the most frequently used pharmacotherapeutic approach in patients infected with hepatitis B virus (HBV). Numerous studies have reported that interleukin-28B (IL-28B) genetic polymorphisms are related to the therapeutic efficacy of PEG-IFN-α, but the results are inconsistent. The present meta-analysis aimed to analyze the association between IL-28B genetic polymorphisms and the prognosis of patients with chronic hepatitis B (CHB) treated with PEG-IFN-α to inform clinical practice.Methods: PubMed, EBSCO, and Scopus databases were searched for relevant literature published before February 30, 2021. We calculated the crude odds ratios (ORs) with 95% confidence intervals (CIs) of the cited articles. A total of 2510 patients with CHB treated with PEG-IFN-α in 13 clinical cohort studies were analyzed.Results: The overall analysis demonstrated a potential association between IL-28B genetic polymorphisms and response to PEG-IFN-α; however, the association was not statistically significant. Furthermore, the subgroup analysis revealed that among patients with HBeAg-negative CHB, the rs12979860 CC genotype and rs8099917 TT genotype were associated with more significant treatment response to PEG-IFN-α (CC vs. non-CC: OR 2.78, 95% CI 1.00–7.76, I2 = 83%; TT vs. non-TT: OR 2.16, 95% CI 1.35–3.48, I2 = 0%). Among Asian patients with CHB, the rs12979860 CC genotype was associated with a more significant treatment response to PEG-IFN (CC vs. non-CC: OR 1.88, 95% CI 1.18–2.99, I2 = 0%).Conclusion: This meta-analysis revealed that the IL-28B rs12979860 CC genotype and rs8099917 TT genotype indicated a better treatment response than non-CC and non-TT genotypes for PEG-IFN-α in patients with CHB.

Сatamnestic data on the effect of interferon therapy on the course of combined HIV/HCV-infection

Aim: catamnestic analysis of the effectiveness of antiviral therapy for chronic hepatitis C in combination with HIV infection.Materials and methods. A retrospective study included 145 patients with combined HCV/HIV infection for 8±0,43 years.Results. 55% of patients received antiviral therapy for chronic hepatitis with pegylated interferons and ribavirin. The frequency of achieving a stable virological response is 73%. Persistent virological response with favorable Il-28B genotypes was detected in 85% of cases, with unfavorable genotypes less frequently — in 63% (p=0,028); the relapse rate is 27%. The level of HIV RNA viral load and the frequency of patients with secondary diseases was higher in patients with natural HCV/HIV infection with favorable interleukin-28B genotypes compared to other comparison groups (р<0,05).Conclusion. The course of chronic hepatitis C after therapy was more positive with favorable Il-28B genotypes. HIV infection was more severe in the absence of antiviral therapy for chronic hepatitis C.

Interleukin-28B dampens protease-induced lung inflammation via IL-25 and TSLP inhibition in epithelial cells

Asthma is a chronic respiratory disease with high heterogeneity in human. Different mouse models have been applied for investigation of pathogenesis and treatment of asthma, which target on different cells, receptors and pathways. Interleukin (IL-) 28B, a member of λ-interferons, have been shown to play a protective role in OVA-induced asthma, which is antigen-specific and adaptive immune system dominant. However, the roles of IL-28B in protease-induced asthma, an adaptive immune system independent asthma, are still unclear. Here, we used plant-derived cysteine protease, papain to induce asthma in mice and found that IL-28B was capable of alleviating papain-induced asthma. Papain challenge lead to activation of epithelial cells and production of alarmin, such as IL-25 and thymic stromal lymphopoietin and IL-28B treatment down-regulated their production. Further mechanism was proved to be that IL-28B inhibited the phosphorylation of Erk in epithelial cells via interaction with their receptors. Our results reveal a protective role of IL-28B via regulation of epithelial cells in protease induced asthma.