Today we are excited to present a Pulmonary Grand Rounds presentation from Daniel S. Chertow, M.D., M.P.H. Dr. Chertow is an Assistant Clinical Investigator in the Critical Care Medicine Department of the NIH and a Special Volunteer in the Viral Pathogenesis and Evolution Section, Laboratory of Infectious Diseases, NIAID. Over the last several years he has solidified his role as a world expert in the field of virology and today speaks on a topic he has published a great deal about, Influenza virus. Tis the season for influenza, and if you ever hope to survive it, you will listen to this talk!  Clinical Pearls * Influenza virus is a SS RNA virus with surface glycoproteins, HA (hemagglutinin) and NA (neuraminidase) * Antigens are made to combat the flu by targeting the HA and NA groups * Antigenic “drift”: the change year to year in the HA groups leading to less immunological protection year to year and a need for new immunizations *  18 HA + 11 NA subtypes, a combination leads to nomenclature and flu types (H1N1, H5N1….) * Nearly all found in birds, some in other species of animals (pigs, etc.) as a reservoir * Pigs and birds are “mixing vessels” that lead to new strains * Vaccines are recommended for all persons ≥ 6 months of age * Recent technology has made them well matched for all circulating strains (including H1N1) * Influenza B is always a guess, no data showing which will surface * Risk factors for severe disease: * >65 yo, <5yo  * Obesity, BMI>40 * Pre-existing Resp/Cardiac/Neuro conditions * Immune suppression * Pregnancy * Sialic acids on respiratory epithelium are the preferred binding surface for influenza virions * Neuraminidase works to make a binding location on influenza- can be targeted for inhibition and thus limit influenza’s virulence * Influenza predisposes to secondary bacterial damage by damaging epithelial airway linings * Starts with bronchiolitis → sloughing of epithelial layer→ necrotic debris * Fills alveoli with proteinaceous materials and inflammatory cells * Exposes binding sites on the basement membrane, increases bacterial adherence, and immune cell dysfunction * Increases morbidity and mortality overall (~death in 7 days) * Bacterial co-infection diagnosis is often delayed or inaccurate as testing is difficult * Clinical judgement predominates * Diagnosis: Rapid antigen tests insensitive (50-70%) * Molecular testing = Gold standard * Collect nasopharyngeal swab/aspirate or a BAL * Synthetic NOT cotton swab (will interfere with the assay) * Collected w/in 7 days of symptom onset (or longer if its a BAL) * Neuraminidase inhibitors (NAI) * 5 metaanalyses, 2 Cochrane reviews- Mixed reviews * In 2014 Munthiri et al.  showed that Neuraminidase inhibitors given earlier led to decreased mortality * Based on this study we are now treating empirically, especially if early in the course. * ICU recommendations: * NAI: * Oseltamivir 75mg PO BID (90-95% successful at viral treatment) * Peramivir IV x 5 days for those unable to tolerate enteral route * Zanamivir IV for those with Oseltamivir resistance (need to contact health officials!