Influenza influences ion channels.

摘要

The symptoms of influenza virus A are multiple and include fever, cough, sore throat, body aches, headache, chills and fatigue. This pathogen is responsible for the seasonal outbreak of the flu, with mild airway involvement and low mortality. However, in a more virulent form (the Spanish flu of 1918) influenza was responsible for some 50-100 million deaths world wide (Taubenberger & Morens, 2006). Influenza virus is transmitted by aerosol; once inhaled, the virus attaches to sialic acid residues on the apical membrane of respiratory epithelia via haemagglutinin present in the viral membrane. Viral content enters the cell where the cell's machinery is utilized to produce more viral particles which then bud from the epithelial cell membrane to infect adjacent cells. In rapidly progressing cases (typically one week) mortality is in part due to viral pneumonia (inflammation and filling of the lung with fluid) and is a consequence of viral-dependent cell necrosis or apoptosis, and an immune response involving leukocytes, cytokines and chemokines, with a resultant accumulation of fluid and cell debris in the alveoli and upper airway spaces. Upper and lower airway epithelia maintain a low fluid volume in the respiratory tract by balancing fluid secretion (active chloride secretion) with fluid absorption (active sodium absorption) (see Sartori & Matthay, 2002). In the lower airways, disruption of the absorptive component, stimulation of the secretory component, or both, can result in fluid accumulation in the alveolar space, increased airway resistance and consequent reduction in blood oxygenation. Fluid absorption occurs by the diffusion of sodium into the cell through apical membrane epithelial sodium channels (ENaCs), the sodium is transported out of the cell across the baso-lateral membrane by the sodium-potassium