Hong Kong Med J 2014;20(Suppl 6):S20-4
Role for autophagy in cellular response to influenza virus infection
AHY Law, DCW Lee, TYY Leon, ASY Lau
Cytokine Biology Group, Department of Paediatrics and Adolescent Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong
1. A differential induction of autophagy was noted between influenza virus A/Hong Kong/54/98 (H1N1) and A/Quail/Hong Kong/G1/97 (H9N2/G1) infections.
2. The H9N2/G1 virus, which shows a delay in apoptosis activation, induces autophagy to a greater extent than the H1N1 virus.
3. Autophagy is not involved in H9N2/G1 virus replication in primary human blood macrophages.
4. Using 3-methyladenine to inhibit autophagy and small interfering RNA to silence the autophagy gene (Atg5), autophagic responses play a role in influenza virus-induced CXCL10 and interferon-_ expression in human macrophages.
2. The H9N2/G1 virus, which shows a delay in apoptosis activation, induces autophagy to a greater extent than the H1N1 virus.
3. Autophagy is not involved in H9N2/G1 virus replication in primary human blood macrophages.
4. Using 3-methyladenine to inhibit autophagy and small interfering RNA to silence the autophagy gene (Atg5), autophagic responses play a role in influenza virus-induced CXCL10 and interferon-_ expression in human macrophages.