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Explore how neutrophils shape the immune response in health and disease. This poster highlights neutrophil pathogen defense mechanisms, including phagocytosis, degranulation, and NETosis, as well as neutrophil roles in inflammation and NET-associated pathologies.
DOWNLOAD NOWSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is an enveloped positive-stranded RNA virus and the causative agent of COVID-19, a primarily respiratory illness characterized by fever, cough, and shortness of breath that can lead to life-threatening complications.1,2,3,4,5 The SARS-CoV-2 genome contains approximately 30 kilobases and 14 open reading frames (ORFs) that encode four structural proteins: spike, envelope, membrane, and nucleocapsid, as well as 16 non-structural proteins and 9 accessory factors.6 SARS-CoV-2 non-structural protein 1 (nsp1) is a multifunctional protein and virulence factor that inhibits host mRNA translation, including translation of antiviral proteins such as IFN-β and IFN-λ1.7,8,9 It is composed of an N-terminal domain and a C-terminal domain connected via an unstructured 20-amino acid residue linker.10,9 The SARS-CoV-2 nsp1 C-terminal domain binds to the mRNA entry site of the 40S subunit of the host ribosome, which prevents host mRNA from entering, while the N-terminal binds to the 40S decoding center preventing accurate alignment of tRNA and mRNA.8,10,9 SARS-CoV-2 nsp1 also induces host mRNA degradation, prevents mRNA export from the nucleus to the cytoplasm, and binds to pre-rRNA in the nucleolus to disrupt rRNA biogenesis.11,9,12,7
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