False color Scanning electron micrograph of<unk>  virus (in orange) budding off an infected cell<unk>  fever is mostly caused by the<unk> . The symptoms include flu-like illness characterized by fever, general weakness, cough, sore throat, headache, and gastrointestinal manifestations. Hemorrhagic manifestations include vascular permeability. Upon entry, the<unk>  infects almost every tissue in the human body. It starts with the mucosa, intestine, lungs and urinary system, and then progresses to the vascular system. The main targets of the virus are antigen-presenting cells, mainly dendritic cells) and endothelial cells. In 2012 it was reported how<unk>  nucleoprotein (NP) sabotages the host's innate immune system response. Generally, when a pathogen enters into a host, innate defense system recognizes the pathogen-associated molecular patterns (PAMP) and activates an immune response. One of the mechanisms detects double stranded RNA (dsRNA), which is only synthesized by negative-sense viruses. In the cytoplasm, dsRNA receptors, such as RIG-I (retinoic acid-inducible gene I) and MDA-5 (melanoma differentiation associated gene 5), detect dsRNAs and initiate signaling pathways that translocate IRF-3 (interferon regulatory factor 3) and other transcription factors to the nucleus. Translocated transcription factors activate expression of interferons 𝛂 and 𝛃, and these initiate adaptive immunity. NP encoded in<unk>  is essential in viral replication and transcription, but it also suppresses host innate IFN response by inhibiting translocation of IRF-3. NP of<unk>  is reported to have an exonuclease activity to only dsRNAs. the NP dsRNA exonuclease activity counteracts IFN responses by digesting the PAMPs thus allowing the virus to evade host immune responses.
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