Research Article, J Virol Antivir Res Vol: 7 Issue: 1
Cathepsin B Plays a Key Role in Optimal Production of the Influenza A- Virus
Macon D Coleman, Soon-Duck Ha, Mansour Haeryfar, Stephen Dominic Barr and Sung Ouk Kim*
Department of Microbiology and Immunology and Center for Human Immunology, Drake Research Institute, Western University, London, Ontario, Canada
*Corresponding Author : Sung Ouk Kim
Department of Microbiology and Immunology and Center for Human Immunology, Siebens-7 Drake Research Institute, Western University, Ontario, Canada
Tel: (519)850-2961
Fax: (519)-661-2046
E-mail: sung.kim@schulich.uwo.ca
Received: November 24, 2017 Accepted: May 04, 2018 Published: May 11, 2018
Citation: Coleman MD, Ha S, Haeryfar M, Barr SD, Kim SO (2018) Cathepsin B Plays a Key Role in Optimal Production of the Influenza A- Virus. J Virol Antivir Res 7:1. doi: 10.4172/2324-8955.1000178
Abstract
Background: Influenza A- virus (IAV) is the etiologic agent of the febrile respiratory illness, commonly referred to as ‘flu’. The lysosomal protease cathepsin B (CTSB) has shown to be involved in the lifecycle of various viruses. Here, we examined the role of CTSB in the IAV lifecycle.
Methods: CTSB-deficient (CTSB -/-) macrophages and the human lung epithelial cell line A549 cells treated with CA-074Me were infected with the A/Puerto Rico/8/34 strain of IAV (IAV- PR8). Viral
entry and propagation were measured through quantitative realtime RT-PCR; production and localization of hemagglutinin (HA) protein in the infected host cells were analysed by Western blots, flow cytometry and confocal microscopy; production of progeny viruses were measured by a hemagglutination assay.
Results: CTSB -/- macrophages and CA-074Me-treated A549 cells had no defects in incorporating IAV-PR8 virions and permitting viral RNA synthesis. However, these cells produced significantly lower amounts of HA protein and progeny virions than wild-type or untreated cells.
Conclusion: These data indicate that CTSB is involved in the expression of IAV-PR8 HA protein and subsequent optimal production of IAV-PR8 progeny virions. Targeting CTSB can be a novel therapeutic strategy for treating IAV infection.