tetano
Editor, Senior Moderator
J Virol Antivir Res. 2018;2018:1-20. doi: 10.4172/2324-8955.1000178.
[h=1]Cathepsin B plays a key role in optimal production of the influenza A virus.[/h] Coleman MD[SUP]1[/SUP], Ha SD[SUP]1[/SUP], Haeryfar SMM[SUP]1[/SUP], Barr SD[SUP]1[/SUP], Kim SO[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] [h=4]Background:[/h] 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.
[h=4]Methods:[/h] CTSB-deficient (CTSB[SUP]-/-[/SUP]) 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 real-time 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.
[h=4]Results:[/h] CTSB[SUP]-/-[/SUP] 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.
[h=4]Conclusion:[/h] 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.
[h=4]KEYWORDS:[/h] CA-074 Me; Cathepsin B; Hemagglutinin; Influenza A virus
PMID: 29349092 PMCID: PMC5770218 DOI: 10.4172/2324-8955.1000178
Free PMC Article
[h=1]Cathepsin B plays a key role in optimal production of the influenza A virus.[/h] Coleman MD[SUP]1[/SUP], Ha SD[SUP]1[/SUP], Haeryfar SMM[SUP]1[/SUP], Barr SD[SUP]1[/SUP], Kim SO[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] [h=4]Background:[/h] 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.
[h=4]Methods:[/h] CTSB-deficient (CTSB[SUP]-/-[/SUP]) 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 real-time 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.
[h=4]Results:[/h] CTSB[SUP]-/-[/SUP] 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.
[h=4]Conclusion:[/h] 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.
[h=4]KEYWORDS:[/h] CA-074 Me; Cathepsin B; Hemagglutinin; Influenza A virus
PMID: 29349092 PMCID: PMC5770218 DOI: 10.4172/2324-8955.1000178
Free PMC Article