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onsdag 15 oktober 2014

How influenza virus is detected in immunesystem by interferons


 Figure 1. Induction and effects of IFN during virus infection.

Virus infection delivers nucleic acids into the cytosol or endosomal compartment. Innate nucleic acid sensors including toll-like receptors (TLRs), RIG-I-like receptors (RLRs) and cytosolic DNA receptors (CDRs) detect these DNAs and RNAs and then trigger a signal transduction cascade that induces IFN. Adaptor proteins, kinases and transcription factors mediate signalling. Note that additional proteins have been implicated and that the figure only shows some selected key components. IFN signals via IFNAR resulting in the induction of interferon-stimulated genes (ISGs) that have direct and indirect anti-viral effects.

Figure 2 RIG-I recognizes the 5’-PPP-bearing influenza A virus RNA genome.

A schematic representation of the flu life cycle is shown. Flu has a segmented genome consisting of eight negative sense RNA molecules carrying 5’-PPP groups. Virus particles enter cells via endocytosis, followed by uncoating and nuclear replication of the viral genome (vRNA). This involves a positive sense anti-genome intermediate (cRNA). The viral genome is also transcribed in the nucleus into capped viral messenger RNAs (mRNAs) that are exported to the cytoplasm and translated. Viral proteins and replicated viral genomes assemble progeny virus particles that bud from the cell surface. IFN induction during flu infection is mediated by RIG-I recognition of progeny viral genomes and signalling via the mitochondrial adaptor protein MAVS. CARD, caspase activation and recruitment domain; Helicase, DExD/H-box RNA helicase domain; RD/CTD, repressive domain, also known as C-terminal domain; TM, transmembrane domain. Figure 2 RIG-I recognizes the 5’-PPP-bearing influenza A virus RNA genome. A schematic ...
The innate immune response is critical for successful host defence against virus infection. Cell-intrinsic mechanisms detect virus presence and signal for the induction of innate response genes such a type I interferons (IFNs). Nucleic acids are often a molecular signature of virus infection and are recognised by innate receptors including toll-like receptors, RIG-I-like receptors and cytosolic DNA receptors (Figure 1). In addition to their protective role in infectious disease, some of these receptors have also been implicated in inflammatory conditions.
Our research dissects the molecular biology of activation and

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