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In this study, we conducted an indirect comparison analysis to compare the efficacy and safety of immune checkpoint inhibitors with those of antiangiogenic therapy—two effective treatment methods for advanced non–small-cell lung cancer (NSCLC). Eligible randomised control trials of immune checkpoint inhibitors, antiangiogenic therapy, and doublet platinum-based therapy published up to July 2017 were comprehensively analysed. Through the indirect comparison analysis of 37 trials involving 16810 patients, treatments were compared for overall survival (OS) and grade 3–5 adverse events. For first-line treatment, the use of pembrolizumab alone (hazard ratio [HR]: 0.6; 95% confidence interval [CI]: 0.4–0.91) and a combination of bevacizumab and doublet platinum-based therapy (HR: 0.86; 95% CI: 0.75–0.99) demonstrated substantial survival benefits compared with doublet platinum-based therapy. For subsequent treatment, nivolumab may provide higher efficacy and lower toxicity than antiangiogenic therapy. Overall, anti-PD1 monoclonal antibodies may be superior to antiangiogenic therapy in terms of OS and grade 3–5 adverse events. This meta-analysis suggests that pembrolizumab and nivolumab might be favourable choices for first-line and subsequent treatment, respectively, for patients with advanced NSCLC. Additional randomised control trials are required for a comprehensive evaluation of the outcomes among regimens.

Autophagy and immune response are two defense systems that human-body uses against viral infection. Previous studies documented that some viral mechanisms circumvented host immunity mechanisms and hijacked autophagy for its replication and survival. Here, we focus on interactions between autophagy mechanism and innate-immune-response in HCV-subgenomic replicon cells to find a mechanism linking the two pathways. We report distinct effects of two autophagy-related protein ATG10s on HCV-subgenomic replication. ATG10, a canonical long isoform in autophagy process, can facilitate HCV-subgenomic replicon amplification by promoting autophagosome formation and by combining with and detaining autophagosomes in cellular periphery, causing impaired autophagy flux. ATG10S, a non-canonical short isoform of ATG10 proteins, can activate expression of IL28A/B and immunity genes related to viral ds-RNA including ddx-58, tlr-3, tlr-7, irf-3 and irf-7, and promote autophagolysosome formation by directly combining and driving autophagosomes to perinuclear region where lysosomes gather, leading to lysosomal degradation of HCV-subgenomic replicon in HepG2 cells. ATG10S also can suppress infectious HCV virion replication in Huh7.5 cells. Another finding is that IL28A protein directly conjugates ATG10S and helps autophagosome docking to lysosomes. ATG10S might be a new host factor against HCV replication, and as a target for screening chemicals with new anti-virus mechanisms.

Studies on the clinical efficacy of influenza vaccination on patients with systemic lupus erythematosus (SLE) are scant. The present study compared the incidence of hospitalization, morbidity, and mortality in patients with SLE between cohorts with and without influenza vaccination. We used the Taiwan’s insurance claims data between 2001 and 2012 for identifying annual adult patients with SLE with (N = 1765) and without (N = 8360) influenza vaccination. The incidence rate ratio and hazard ratio (HR) for morbidities and mortality were measured for the vaccine and nonvaccine cohorts. The vaccine cohort had a lower hospitalization rate than did the nonvaccine cohort, with an adjusted HR of 0.82 (95% CI 0.73–0.92). Furthermore, the vaccine cohort was less likely to be admitted to the intensive care unit [adjusted HR 0.55 (95% CI 0.39–0.79)], to be hospitalized for septicemia, bacteremia, or viremia [adjusted HR 0.48 (95% CI 0.32–0.73)], to undergo in-hospital dialysis [adjusted HR 0.40 (95% CI 0.20–0.81)], and were less predisposed to death [adjusted HR 0.41 (95% CI 0.27–0.61)]. In conclusion, influenza vaccination in patients with SLE is associated with a reduced risk of morbidity and mortality.

The cluster of differentiation 36 (CD36) is a membrane protein related to lipid metabolism. We show that HCV infection in vitro increased CD36 expression in either surface or soluble form. HCV attachment was facilitated through a direct interaction between CD36 and HCV E1 protein, causing enhanced entry and replication. The HCV co-receptor effect of CD36 was independent of that of SR-BI. CD36 monoclonal antibodies neutralized the effect of CD36 and reduced HCV replication. CD36 inhibitor sulfo-N-succinimidyl oleate (SSO), which directly bound CD36 but not SR-BI, significantly interrupted HCV entry, and therefore inhibited HCV replication. SSO’s antiviral effect was seen only in HCV but not in other viruses. SSO in combination with known anti-HCV drugs showed additional inhibition against HCV. SSO was considerably safe in mice. Conclusively, CD36 interacts with HCV E1 and might be a co-receptor specific for HCV entry; thus, CD36 could be a potential drug target against HCV.

Kawasaki disease (KD) is an acute, inflammatory and self-limited vasculitis affecting infants and young children. Coronary artery aneurysm (CAA) formation is the major complication of KD and the leading cause of acquired cardiovascular disease among children. To identify susceptible loci that might predispose patients with KD to CAA formation, a genome-wide association screen was performed in a Taiwanese KD cohort. Patients with both KD and CAA had longer fever duration and delayed intravenous immunoglobulin treatment time. After adjusting for these factors, 100 susceptibility loci were identified. Four genes were identified from a single cluster of 35 using the Ingenuity Pathway Analysis (IPA) Knowledge Base. Silencing KCNQ5, PLCB1, PLCB4 and PLCL1 inhibited the effect of lipopolysaccharide-induced endothelial cell inflammation with varying degrees of proinflammatory cytokine expression. PLCB1 showed the most significant inhibition. Endothelial cell inflammation was also inhibited by using a phospholipase C (PLC) inhibitor. The single nucleotide polymorphism rs6140791 was identified between PLCB4 and PLCB1. Plasma PLC levels were higher in patients with KD and CC+CG rs6140791genotypes and these genotypes were more prevalent in patients with KD who also had CAA. Our results suggest that polymorphism of the PLCB4/B1 genes might be involved in the CAA pathogenesis of KD.