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Background and ObjectiveThe impact of perioperative allogenenic blood transfusion (ABT) on clinical outcomes for hepatocellular carcinoma (HCC) is conflicting and unclear. The aim of this meta-analysis is to evaluate the association between ABT and HCC clinical outcomes. Outcomes evaluated were all-cause death, tumor recurrence and postoperative complications.MethodsRelevant articles were identified through MEDLINE search (up to November 2012). Meta-analyses were performed by using the fixed or random effect models. Study heterogeneity was assessed by Q-test and I2 test. Publication bias was evaluated by funnel plots, Egger′s and Begg’s test.ResultsA total of 5635 cases from 22 studies finally met our inclusion criteria. Meta-analysis indicated HCC patients with ABT had an increased risk of all-cause death at 3 and 5 years after surgery (respectively: OR = 1.92, 95% CI, 1.61–2.29,P<0.001; OR = 1.60, 95% CI, 1.47–1.73,P<0.001 ) compared with those without ABT. The risk of tumor recurrence was significantly higher for ABT cases at 1, 3 and 5 years (respectively: OR = 1.70, 95% CI, 1.38–2.10, P<0.001; OR = 1.22, 95% CI, 1.08–1.38, P<0.001; OR = 1.16, 95% CI, 1.08–1.24, P<0.001). The HCC cases with ABT significantly increased postoperative complications occurrence compared with non-ABT cases (OR = 1.78,95% CI, 1.34–2.37, P<0.001).ConclusionsThe findings from the current meta-analysis demonstrated that ABT was associated with adverse clinical outcomes for HCC patients undergoing surgery, including increased death, recurrence and complications. Therefore, ABT should not be performed if possible.

The innate immune system initiates immune responses by pattern-recognition receptors (PRR). Virus-derived nucleic acids are sensed by the retinoic acid-inducible gene I (RIG-I)-like receptor (RLR) family and the toll-like receptor (TLR) family as well as the DNA sensor cyclic GMP-AMP (cGAMP) synthase (cGAS). These receptors activate IRF3/7 and NF-κB signaling pathways to induce the expression of type I interferons (IFNs) and other cytokines firing antiviral responses within the cell. However, to achieve a favorable outcome for the host, a balanced production of IFNs and activation of antiviral responses is required. Posttranslational modifications (PTMs), such as the covalent linkage of functional groups to amino acid chains, are crucial for this immune homeostasis in antiviral responses. Canonical PTMs including phosphorylation and ubiquitination have been extensively studied and other PTMs such as methylation, acetylation, SUMOylation, ADP-ribosylation and glutamylation are being increasingly implicated in antiviral innate immunity. Here we summarize our recent understanding of the most important PTMs regulating the antiviral innate immune response, and their role in virus-related immune pathogenesis.Keywords: Antiviral immunity r Interferons r Phosphorylation r Post-translational modifications r PRR r Ubiquitination IntroductionInfectious diseases, especially virus infections, are still a serious threat to humanity and the host innate immune system represents a critical defense against invading viruses. Host cells can initiate these innate immune responses by detecting viral DNA and RNA with a set of pattern recognition receptors (PRRs) including the toll-like receptor (TLR) family and the retinoic acid-inducible gene I (RIG-I)-like receptor (RLR) family, as well as cytosolic DNA sensors such as cyclic GMP-AMP (cGAMP) synthase (cGAS), IFI16 and DDX41 [1,2]. After recognition of viral nucleic acids, these PRRs trigger the production of proinflammatory cytokines, chemokines and type I interferons (IFNs), which subsequently induce synthesis of antiviral proteins, death of infected cells and activation of the adaptive immune response [3,4]. These antiviral signals Correspondence: Dr. Baoxue Ge e-mail: gebaoxue@sibs.ac.cn must be spatially and temporally orchestrated to achieve an optimal outcome for the host and much attention has been raised to understanding the signaling pathways and regulatory factors in the antiviral innate immunity.Toll-like receptors, including TLR3, TLR7, TLR8 and TLR9, sense endosomal nucleic acids derived from the enclosed microbes and infected apoptotic cells. While TLR9 detects unmethylated CpG DNA species, TLR3 and TLR7/8 recognize double-stranded RNA (dsRNA) and single-stranded RNA (ssRNA), respectively [5] ( Fig. 1). Following ligand binding, the TLRs form a signaling platform in which distinct Toll/interleukin-1 receptor (TIR) domaincontaining adaptors are engaged. For instance, TLR3 signals via TIR-domain-containing adaptor protein inducing interferon beta (TRIF), and TLR7/8/9 rel...