Prion Protein is a Novel Modulator of Influenza: Potential Implications for Anti-Influenza Therapeutics.
Identifieur interne : 000255 ( Main/Exploration ); précédent : 000254; suivant : 000256Prion Protein is a Novel Modulator of Influenza: Potential Implications for Anti-Influenza Therapeutics.
Auteurs : Suehiro Sakaguchi [Japon] ; Junji Chida [Japon]Source :
- Current issues in molecular biology [ 1467-3045 ] ; 2020.
Abstract
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, PrPC, whose conformational conversion into the amyloidogenic isoform, PrPSc, 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 PrPC-knockout mice, suggesting that the anti-oxidative activity of PrPC is probably attributable to its function of activating SOD1 through regulating Cu content in lungs. Here, we introduce PrPC 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.
DOI: 10.21775/cimb.037.021
PubMed: 31814573
Affiliations:
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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.</div></front></TEI><affiliations><list><country><li>Japon</li></country></list><tree><country name="Japon"><noRegion><name sortKey="Sakaguchi, Suehiro" sort="Sakaguchi, Suehiro" uniqKey="Sakaguchi S" first="Suehiro" last="Sakaguchi">Suehiro Sakaguchi</name></noRegion><name sortKey="Chida, Junji" sort="Chida, Junji" uniqKey="Chida J" first="Junji" last="Chida">Junji Chida</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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