Role for autophagy in cellular response to influenza virus infection.

The outbreak of avian influenza A (H5N1/97) virus infection in Hong Kong is the first documented case of direct transmission of the H5N1 virus from birds to humans. The high mortality rate of >60% caused great concern to the public and government. In addition, avian influenza H9N2 viruses have become highly prevalent in poultry in many countries and have caused human infections. The high prevalence, wide geographic range, rapid evolution, and frequent reassortment of H9N2 viruses in poultry,1 combined with the increasing number of avian influenza infections in humans, highlights their pandemic and zoonotic potential. Apoptosis and autophagy constitute the two processes through which superfluous, damaged, or aged cells or organelles are eliminated.2 Apoptosis has been shown to be one of the most effective host defence mechanisms against microbial pathogens. The cell death process results in inhibition of virus replication, limitation of virus dissemination, and minimisation of uncontrolled inflammatory responses. Avian influenza (H5N1/97) and its precursors trigger a caspase-dependent but delayed apoptotic response in human macrophages, compared with human influenza viruses (H1N1 and H3N2).3 Autophagy is a tightly regulated cellular homeostatic process involving the sequestration of parts of the cytosol and intracellular organelles within double-membraned autophagic vacuoles that are delivered to lysosomes for degradation. Autophagy plays essential roles in physiological processes such as cellular responses to starvation, Hong Kong Med J 2014;20(Suppl 6):S20-4 RFCID project number: 09080832 AHY Law, DCW Lee, TYY Leon, ASY Lau *