PKR and TLR3 trigger distinct signals that coordinate the induction of antiviral apoptosis.

RIG-I-like receptors (RLRs), protein kinase R (PKR), and endosomal Toll-like receptor 3 (TLR3) sense viral non-self RNA and are involved in cell fate determination. However, the mechanisms by which intracellular RNA induces apoptosis, particularly the role of each RNA sensor, remain unclear. We performed cytoplasmic injections of different types of RNA and elucidated the molecular mechanisms underlying viral dsRNA-induced apoptosis.

Adsorptive Inhibition of Enveloped Viruses and Nonenveloped Cardioviruses by Antiviral Lignin Produced from Sugarcane Bagasse via Microwave Glycerolysis.

Antiviral lignin was produced by acidic microwave glycerolysis of sugarcane bagasse. The lignin exhibited antiviral activity against nonenveloped (encephalomyocarditis virus (EMCV) and Theiler's murine encephalomyelitis virus (TMEV)) and enveloped (vesicular stomatitis virus (VSV), Sindbis virus (SINV), and Newcastle disease virus (NDV)) viruses. A series of lignins with different antiviral activities were prepared by reacting bagasse at 140, 160, 180, and 200 °C to analyze the antiviral mechanism.

Ubiquitin-Dependent and -Independent Roles of E3 Ligase RIPLET in Innate Immunity.

The conventional view posits that E3 ligases function primarily through conjugating ubiquitin (Ub) to their substrate molecules. We report here that RIPLET, an essential E3 ligase in antiviral immunity, promotes the antiviral signaling activity of the viral RNA receptor RIG-I through both Ub-dependent and -independent manners. RIPLET uses its dimeric structure and a bivalent binding mode to preferentially recognize and ubiquitinate RIG-I pre-oligomerized on dsRNA.

A Plant-Derived Nucleic Acid Reconciles Type I IFN and a Pyroptotic-like Event in Immunity against Respiratory Viruses.

Nucleic acids carrying pathogen-associated molecular patterns trigger innate immune responses and are used to activate host immunity. Although synthetic nucleic acids have been used for that purpose, they have shown limitations for in vivo and clinical applications. To address this issue, we tested a naturally occurring dsRNA extracted from rice bran (rb-dsRNA) and characterized it as a potent ligand of TLR3 and MDA5.

RIG-I-Like Receptors and Type I Interferonopathies.

Type I interferon (IFN) production by the proper activation of nucleic acid sensors is essential for hosts to eliminate invading viruses. Among these sensors, RIG-I-like receptors (RLRs) are well-known viral RNA sensors in the cytoplasm that recognize the nonself signatures of viral RNAs to trigger IFN responses. Recent accumulating evidence has clarified that some specific and atypical self-RNAs also cause activation of RLRs independently of virus infection.

Leader-Containing Uncapped Viral Transcript Activates RIG-I in Antiviral Stress Granules.

RIG-I triggers antiviral responses by recognizing viral RNA (vRNA) in the cytoplasm. However, the spatio-temporal dynamics of vRNA sensing and signal transduction remain elusive. We investigated the time course of events in cells infected with Newcastle disease virus (NDV), a non-segmented negative-strand RNA virus.

[The anaylsis of mortality rate according to CTP score and MELD score in patients with liver cirrhosis].

Background/aims: The Model for End-Stage Liver Disease (MELD) consists of serum bilirubin and creatinine levels, International Normalized Ratio (INR) for prothrombin time, and etiology of liver disease. The MELD score is a reliable measurement of mortality risk and is suitable for a disease severity index in patients with end-stage liver disease. We examined the validity of the MELD as a disease severity index for patients with end-stage liver disease.