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  • Respiratory Syncytial Virus
    • history and brief epidemiology
      • RSV is the most common cause of respiratory infection in infants and young children
      • Virtually all infected by age 2
      • Reinfected throughout life
      • Very young, very old and immunocompromised most at risk
    • Virology
      • an enveloped, neg-sense, ssRNA virus
      • divided into 2 subtypes A and B (based on F and G protein)
      • Virions are pleomorphic 10 genes encoding 11 proteins
        • multiple different shapes
    • RSV diagnosis and treatment
      • PCR and rapid antigen tests
      • treatment = isolation
      • no vaccine and no treatment
      • one prophylactic- palivizumab (monocolonal antibody)
    • Pathogenesis
      • causes syncytia
      • Runny nose, cough and wheeze
      • Infection results in inflammation, infiltration of inflammatory cells
        • (neutrophils, monocytes), increased mucous production, sloughed cells.
    • Innate antiviral mechanisms
      • Cell apoptosis. Extrinsic: TRAIL binding to death receptor 4/5Intrinsic: BCL-2 proteins localising to mitochondria
      • Cell Stress ER stress Transcriptional stress Oxidative stress
      • Innate immune responses
        • Virus recognised through NOD-like receptors (NLRs), Toll-like receptors (TLRs), RIG-I-like receptors (RLRs)
        • Signal through adapter proteins to activate interferon regulatory factors (IRFs) and NF-kB
        • Type I and type III Interferon and other cytokines produced
          • RSV can be sensed by: RIG-I, MDA5, NOD2. Which signal through mitochondrial antiviral signalling protein (MAVS)TLRs (2, 4, 6 on cell membrane; 3 and 7 on endosomal membranes) signal via MyD88 or TRIF.
          • Activation of IRFs and NF-kB to induce interferons (and other cytokines). IFNs bind to receptors and activate the JAK-STAT pathway resulting in hundreds of ISGs


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