tetano
Editor, Senior Moderator
Curr Issues Mol Biol. 2019 Dec 9;37:21-32. doi: 10.21775/cimb.037.021. [Epub ahead of print] [h=1]Prion Protein is a Novel Modulator of Influenza: Potential Implications for Anti-Influenza Therapeutics.[/h]
Sakaguchi S[SUP]1[/SUP], Chida J[SUP]1[/SUP].
[h=3]Author information[/h] 1 Division of Molecular Neurobiology, Institute for Enzyme Research (KOSOKEN), Tokushima University, 3-18-15 Kuramoto, Tokushima 770-8503, Japan.
[h=3]Abstract[/h] Worldwide spread of influenza A virus (IAV) strains, which are resistant to currently available anti- influenza agents such as viral neuraminidase inhibitors, has encouraged identification of new target molecules for anti-influenza agents. Reactive oxygen species (ROS) causing oxidative stress play a pivotal role in the pathogenesis of lung injuries induced by infection with IAVs, therefore suggesting that anti-oxidative therapeutics targeting cellular molecules could be beneficial against IAV infection without inducing drug-resistant IAV strains. We recently found that the normal cellular prion protein, PrP[SUP]C[/SUP], whose conformational conversion into the amyloidogenic isoform, PrP[SUP]Sc[/SUP], in the brain is a key pathogenic event in prion diseases, is expressed by lung epithelial cells and exerts a protective role against IAV infection in mice by reducing ROS in infected lungs. The Cu content and activity of anti- oxidative enzyme Cu/Zn-superoxide dismutase, or SOD1, were lower in the lungs of PrP[SUP]C[/SUP]-knockout mice, suggesting that the anti-oxidative activity of PrP[SUP]C[/SUP] is probably attributable to its function of activating SOD1 through regulating Cu content in lungs. Here, we introduce PrP[SUP]C[/SUP] as a novel modulator of influenza and its potential implication for anti-oxidative therapies for IAV infection. We also introduce other candidate targets reported for anti- oxidative anti-influenza therapies.
PMID: 31814573 DOI: 10.21775/cimb.037.021
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Sakaguchi S[SUP]1[/SUP], Chida J[SUP]1[/SUP].
[h=3]Author information[/h] 1 Division of Molecular Neurobiology, Institute for Enzyme Research (KOSOKEN), Tokushima University, 3-18-15 Kuramoto, Tokushima 770-8503, Japan.
[h=3]Abstract[/h] Worldwide spread of influenza A virus (IAV) strains, which are resistant to currently available anti- influenza agents such as viral neuraminidase inhibitors, has encouraged identification of new target molecules for anti-influenza agents. Reactive oxygen species (ROS) causing oxidative stress play a pivotal role in the pathogenesis of lung injuries induced by infection with IAVs, therefore suggesting that anti-oxidative therapeutics targeting cellular molecules could be beneficial against IAV infection without inducing drug-resistant IAV strains. We recently found that the normal cellular prion protein, PrP[SUP]C[/SUP], whose conformational conversion into the amyloidogenic isoform, PrP[SUP]Sc[/SUP], in the brain is a key pathogenic event in prion diseases, is expressed by lung epithelial cells and exerts a protective role against IAV infection in mice by reducing ROS in infected lungs. The Cu content and activity of anti- oxidative enzyme Cu/Zn-superoxide dismutase, or SOD1, were lower in the lungs of PrP[SUP]C[/SUP]-knockout mice, suggesting that the anti-oxidative activity of PrP[SUP]C[/SUP] is probably attributable to its function of activating SOD1 through regulating Cu content in lungs. Here, we introduce PrP[SUP]C[/SUP] as a novel modulator of influenza and its potential implication for anti-oxidative therapies for IAV infection. We also introduce other candidate targets reported for anti- oxidative anti-influenza therapies.
PMID: 31814573 DOI: 10.21775/cimb.037.021
Free full text