Vitisin B inhibits influenza A virus replication by multi-targeting neuraminidase and virus-induced oxidative stress

The development of drug-resistant influenza and new pathogenic virus strains underscores the need for antiviral therapeutics. Currently, neuraminidase (NA) inhibitors are commonly used antiviral drugs approved by the US Food and Drug Administration (FDA) for the prevention and treatment of influenza...
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Gespeichert in:

Autor*in:	Eun-Bin Kwon [verfasserIn] Wei Li [verfasserIn] Young Soo Kim [verfasserIn] Buyun Kim [verfasserIn] Hwan-Suck Chung [verfasserIn] Younghoon Go [verfasserIn] Hyun-Jeong Ko [verfasserIn] Jae-Hyoung Song [verfasserIn] Young Ho Kim [verfasserIn] Chun Whan Choi [verfasserIn] Jang-Gi Choi [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	Influenza Vitisin B Vitis vinifera L. Neuraminidase Reactive oxygen species NF-κB

Übergeordnetes Werk:	In: Acta Pharmaceutica Sinica B - Elsevier, 2013, 13(2023), 1, Seite 174-191
Übergeordnetes Werk:	volume:13 ; year:2023 ; number:1 ; pages:174-191

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1016/j.apsb.2022.07.001

Katalog-ID:	DOAJ081075804

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520			\|a The development of drug-resistant influenza and new pathogenic virus strains underscores the need for antiviral therapeutics. Currently, neuraminidase (NA) inhibitors are commonly used antiviral drugs approved by the US Food and Drug Administration (FDA) for the prevention and treatment of influenza. Here, we show that vitisin B (VB) inhibits NA activity and suppresses H1N1 viral replication in MDCK and A549 cells. Reactive oxygen species (ROS), which frequently occur during viral infection, increase virus replication by activating the NF-κB signaling pathway, downmodulating glucose-6-phosphate dehydrogenase (G6PD) expression, and decreasing the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant response activity. VB decreased virus-induced ROS generation by increasing G6PD expression and Nrf2 activity, and inhibiting NF-κB translocation to the nucleus through IKK dephosphorylation. In addition, VB reduced body weight loss, increased survival, decreased viral replication and the inflammatory response in the lungs of influenza A virus (IAV)-infected mice. Taken together, our results indicate that VB is a promising therapeutic candidate against IAV infection, complements existing drug limitations targeting viral NA. It modulated the intracellular ROS by G6PD, Nrf2 antioxidant response pathway, and NF-κB signaling pathway. These results demonstrate the feasibility of a multi-targeting drug strategy, providing new approaches for drug discovery against IAV infection.
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allfields	10.1016/j.apsb.2022.07.001 doi (DE-627)DOAJ081075804 (DE-599)DOAJ7c046e5532d14f3ca54a8fdd2001d638 DE-627 ger DE-627 rakwb eng RM1-950 Eun-Bin Kwon verfasserin aut Vitisin B inhibits influenza A virus replication by multi-targeting neuraminidase and virus-induced oxidative stress 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The development of drug-resistant influenza and new pathogenic virus strains underscores the need for antiviral therapeutics. Currently, neuraminidase (NA) inhibitors are commonly used antiviral drugs approved by the US Food and Drug Administration (FDA) for the prevention and treatment of influenza. Here, we show that vitisin B (VB) inhibits NA activity and suppresses H1N1 viral replication in MDCK and A549 cells. Reactive oxygen species (ROS), which frequently occur during viral infection, increase virus replication by activating the NF-κB signaling pathway, downmodulating glucose-6-phosphate dehydrogenase (G6PD) expression, and decreasing the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant response activity. VB decreased virus-induced ROS generation by increasing G6PD expression and Nrf2 activity, and inhibiting NF-κB translocation to the nucleus through IKK dephosphorylation. In addition, VB reduced body weight loss, increased survival, decreased viral replication and the inflammatory response in the lungs of influenza A virus (IAV)-infected mice. Taken together, our results indicate that VB is a promising therapeutic candidate against IAV infection, complements existing drug limitations targeting viral NA. It modulated the intracellular ROS by G6PD, Nrf2 antioxidant response pathway, and NF-κB signaling pathway. These results demonstrate the feasibility of a multi-targeting drug strategy, providing new approaches for drug discovery against IAV infection. Influenza Vitisin B Vitis vinifera L. Neuraminidase Reactive oxygen species NF-κB Therapeutics. Pharmacology Wei Li verfasserin aut Young Soo Kim verfasserin aut Buyun Kim verfasserin aut Hwan-Suck Chung verfasserin aut Younghoon Go verfasserin aut Hyun-Jeong Ko verfasserin aut Jae-Hyoung Song verfasserin aut Young Ho Kim verfasserin aut Chun Whan Choi verfasserin aut Jang-Gi Choi verfasserin aut In Acta Pharmaceutica Sinica B Elsevier, 2013 13(2023), 1, Seite 174-191 (DE-627)670211095 (DE-600)2631779-5 22113843 nnns volume:13 year:2023 number:1 pages:174-191 https://doi.org/10.1016/j.apsb.2022.07.001 kostenfrei https://doaj.org/article/7c046e5532d14f3ca54a8fdd2001d638 kostenfrei http://www.sciencedirect.com/science/article/pii/S2211383522003124 kostenfrei https://doaj.org/toc/2211-3835 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2023 1 174-191
spelling	10.1016/j.apsb.2022.07.001 doi (DE-627)DOAJ081075804 (DE-599)DOAJ7c046e5532d14f3ca54a8fdd2001d638 DE-627 ger DE-627 rakwb eng RM1-950 Eun-Bin Kwon verfasserin aut Vitisin B inhibits influenza A virus replication by multi-targeting neuraminidase and virus-induced oxidative stress 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The development of drug-resistant influenza and new pathogenic virus strains underscores the need for antiviral therapeutics. Currently, neuraminidase (NA) inhibitors are commonly used antiviral drugs approved by the US Food and Drug Administration (FDA) for the prevention and treatment of influenza. Here, we show that vitisin B (VB) inhibits NA activity and suppresses H1N1 viral replication in MDCK and A549 cells. Reactive oxygen species (ROS), which frequently occur during viral infection, increase virus replication by activating the NF-κB signaling pathway, downmodulating glucose-6-phosphate dehydrogenase (G6PD) expression, and decreasing the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant response activity. VB decreased virus-induced ROS generation by increasing G6PD expression and Nrf2 activity, and inhibiting NF-κB translocation to the nucleus through IKK dephosphorylation. In addition, VB reduced body weight loss, increased survival, decreased viral replication and the inflammatory response in the lungs of influenza A virus (IAV)-infected mice. Taken together, our results indicate that VB is a promising therapeutic candidate against IAV infection, complements existing drug limitations targeting viral NA. It modulated the intracellular ROS by G6PD, Nrf2 antioxidant response pathway, and NF-κB signaling pathway. These results demonstrate the feasibility of a multi-targeting drug strategy, providing new approaches for drug discovery against IAV infection. Influenza Vitisin B Vitis vinifera L. Neuraminidase Reactive oxygen species NF-κB Therapeutics. Pharmacology Wei Li verfasserin aut Young Soo Kim verfasserin aut Buyun Kim verfasserin aut Hwan-Suck Chung verfasserin aut Younghoon Go verfasserin aut Hyun-Jeong Ko verfasserin aut Jae-Hyoung Song verfasserin aut Young Ho Kim verfasserin aut Chun Whan Choi verfasserin aut Jang-Gi Choi verfasserin aut In Acta Pharmaceutica Sinica B Elsevier, 2013 13(2023), 1, Seite 174-191 (DE-627)670211095 (DE-600)2631779-5 22113843 nnns volume:13 year:2023 number:1 pages:174-191 https://doi.org/10.1016/j.apsb.2022.07.001 kostenfrei https://doaj.org/article/7c046e5532d14f3ca54a8fdd2001d638 kostenfrei http://www.sciencedirect.com/science/article/pii/S2211383522003124 kostenfrei https://doaj.org/toc/2211-3835 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2023 1 174-191
allfields_unstemmed	10.1016/j.apsb.2022.07.001 doi (DE-627)DOAJ081075804 (DE-599)DOAJ7c046e5532d14f3ca54a8fdd2001d638 DE-627 ger DE-627 rakwb eng RM1-950 Eun-Bin Kwon verfasserin aut Vitisin B inhibits influenza A virus replication by multi-targeting neuraminidase and virus-induced oxidative stress 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The development of drug-resistant influenza and new pathogenic virus strains underscores the need for antiviral therapeutics. Currently, neuraminidase (NA) inhibitors are commonly used antiviral drugs approved by the US Food and Drug Administration (FDA) for the prevention and treatment of influenza. Here, we show that vitisin B (VB) inhibits NA activity and suppresses H1N1 viral replication in MDCK and A549 cells. Reactive oxygen species (ROS), which frequently occur during viral infection, increase virus replication by activating the NF-κB signaling pathway, downmodulating glucose-6-phosphate dehydrogenase (G6PD) expression, and decreasing the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant response activity. VB decreased virus-induced ROS generation by increasing G6PD expression and Nrf2 activity, and inhibiting NF-κB translocation to the nucleus through IKK dephosphorylation. In addition, VB reduced body weight loss, increased survival, decreased viral replication and the inflammatory response in the lungs of influenza A virus (IAV)-infected mice. Taken together, our results indicate that VB is a promising therapeutic candidate against IAV infection, complements existing drug limitations targeting viral NA. It modulated the intracellular ROS by G6PD, Nrf2 antioxidant response pathway, and NF-κB signaling pathway. These results demonstrate the feasibility of a multi-targeting drug strategy, providing new approaches for drug discovery against IAV infection. Influenza Vitisin B Vitis vinifera L. Neuraminidase Reactive oxygen species NF-κB Therapeutics. Pharmacology Wei Li verfasserin aut Young Soo Kim verfasserin aut Buyun Kim verfasserin aut Hwan-Suck Chung verfasserin aut Younghoon Go verfasserin aut Hyun-Jeong Ko verfasserin aut Jae-Hyoung Song verfasserin aut Young Ho Kim verfasserin aut Chun Whan Choi verfasserin aut Jang-Gi Choi verfasserin aut In Acta Pharmaceutica Sinica B Elsevier, 2013 13(2023), 1, Seite 174-191 (DE-627)670211095 (DE-600)2631779-5 22113843 nnns volume:13 year:2023 number:1 pages:174-191 https://doi.org/10.1016/j.apsb.2022.07.001 kostenfrei https://doaj.org/article/7c046e5532d14f3ca54a8fdd2001d638 kostenfrei http://www.sciencedirect.com/science/article/pii/S2211383522003124 kostenfrei https://doaj.org/toc/2211-3835 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2023 1 174-191
allfieldsGer	10.1016/j.apsb.2022.07.001 doi (DE-627)DOAJ081075804 (DE-599)DOAJ7c046e5532d14f3ca54a8fdd2001d638 DE-627 ger DE-627 rakwb eng RM1-950 Eun-Bin Kwon verfasserin aut Vitisin B inhibits influenza A virus replication by multi-targeting neuraminidase and virus-induced oxidative stress 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The development of drug-resistant influenza and new pathogenic virus strains underscores the need for antiviral therapeutics. Currently, neuraminidase (NA) inhibitors are commonly used antiviral drugs approved by the US Food and Drug Administration (FDA) for the prevention and treatment of influenza. Here, we show that vitisin B (VB) inhibits NA activity and suppresses H1N1 viral replication in MDCK and A549 cells. Reactive oxygen species (ROS), which frequently occur during viral infection, increase virus replication by activating the NF-κB signaling pathway, downmodulating glucose-6-phosphate dehydrogenase (G6PD) expression, and decreasing the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant response activity. VB decreased virus-induced ROS generation by increasing G6PD expression and Nrf2 activity, and inhibiting NF-κB translocation to the nucleus through IKK dephosphorylation. In addition, VB reduced body weight loss, increased survival, decreased viral replication and the inflammatory response in the lungs of influenza A virus (IAV)-infected mice. Taken together, our results indicate that VB is a promising therapeutic candidate against IAV infection, complements existing drug limitations targeting viral NA. It modulated the intracellular ROS by G6PD, Nrf2 antioxidant response pathway, and NF-κB signaling pathway. These results demonstrate the feasibility of a multi-targeting drug strategy, providing new approaches for drug discovery against IAV infection. Influenza Vitisin B Vitis vinifera L. Neuraminidase Reactive oxygen species NF-κB Therapeutics. Pharmacology Wei Li verfasserin aut Young Soo Kim verfasserin aut Buyun Kim verfasserin aut Hwan-Suck Chung verfasserin aut Younghoon Go verfasserin aut Hyun-Jeong Ko verfasserin aut Jae-Hyoung Song verfasserin aut Young Ho Kim verfasserin aut Chun Whan Choi verfasserin aut Jang-Gi Choi verfasserin aut In Acta Pharmaceutica Sinica B Elsevier, 2013 13(2023), 1, Seite 174-191 (DE-627)670211095 (DE-600)2631779-5 22113843 nnns volume:13 year:2023 number:1 pages:174-191 https://doi.org/10.1016/j.apsb.2022.07.001 kostenfrei https://doaj.org/article/7c046e5532d14f3ca54a8fdd2001d638 kostenfrei http://www.sciencedirect.com/science/article/pii/S2211383522003124 kostenfrei https://doaj.org/toc/2211-3835 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2023 1 174-191
allfieldsSound	10.1016/j.apsb.2022.07.001 doi (DE-627)DOAJ081075804 (DE-599)DOAJ7c046e5532d14f3ca54a8fdd2001d638 DE-627 ger DE-627 rakwb eng RM1-950 Eun-Bin Kwon verfasserin aut Vitisin B inhibits influenza A virus replication by multi-targeting neuraminidase and virus-induced oxidative stress 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The development of drug-resistant influenza and new pathogenic virus strains underscores the need for antiviral therapeutics. Currently, neuraminidase (NA) inhibitors are commonly used antiviral drugs approved by the US Food and Drug Administration (FDA) for the prevention and treatment of influenza. Here, we show that vitisin B (VB) inhibits NA activity and suppresses H1N1 viral replication in MDCK and A549 cells. Reactive oxygen species (ROS), which frequently occur during viral infection, increase virus replication by activating the NF-κB signaling pathway, downmodulating glucose-6-phosphate dehydrogenase (G6PD) expression, and decreasing the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant response activity. VB decreased virus-induced ROS generation by increasing G6PD expression and Nrf2 activity, and inhibiting NF-κB translocation to the nucleus through IKK dephosphorylation. In addition, VB reduced body weight loss, increased survival, decreased viral replication and the inflammatory response in the lungs of influenza A virus (IAV)-infected mice. Taken together, our results indicate that VB is a promising therapeutic candidate against IAV infection, complements existing drug limitations targeting viral NA. It modulated the intracellular ROS by G6PD, Nrf2 antioxidant response pathway, and NF-κB signaling pathway. These results demonstrate the feasibility of a multi-targeting drug strategy, providing new approaches for drug discovery against IAV infection. Influenza Vitisin B Vitis vinifera L. Neuraminidase Reactive oxygen species NF-κB Therapeutics. Pharmacology Wei Li verfasserin aut Young Soo Kim verfasserin aut Buyun Kim verfasserin aut Hwan-Suck Chung verfasserin aut Younghoon Go verfasserin aut Hyun-Jeong Ko verfasserin aut Jae-Hyoung Song verfasserin aut Young Ho Kim verfasserin aut Chun Whan Choi verfasserin aut Jang-Gi Choi verfasserin aut In Acta Pharmaceutica Sinica B Elsevier, 2013 13(2023), 1, Seite 174-191 (DE-627)670211095 (DE-600)2631779-5 22113843 nnns volume:13 year:2023 number:1 pages:174-191 https://doi.org/10.1016/j.apsb.2022.07.001 kostenfrei https://doaj.org/article/7c046e5532d14f3ca54a8fdd2001d638 kostenfrei http://www.sciencedirect.com/science/article/pii/S2211383522003124 kostenfrei https://doaj.org/toc/2211-3835 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2023 1 174-191
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topic_facet	Influenza Vitisin B Vitis vinifera L. Neuraminidase Reactive oxygen species NF-κB Therapeutics. Pharmacology
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authorswithroles_txt_mv	Eun-Bin Kwon @@aut@@ Wei Li @@aut@@ Young Soo Kim @@aut@@ Buyun Kim @@aut@@ Hwan-Suck Chung @@aut@@ Younghoon Go @@aut@@ Hyun-Jeong Ko @@aut@@ Jae-Hyoung Song @@aut@@ Young Ho Kim @@aut@@ Chun Whan Choi @@aut@@ Jang-Gi Choi @@aut@@
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callnumber-first	R - Medicine
author	Eun-Bin Kwon
spellingShingle	Eun-Bin Kwon misc RM1-950 misc Influenza misc Vitisin B misc Vitis vinifera L. misc Neuraminidase misc Reactive oxygen species misc NF-κB misc Therapeutics. Pharmacology Vitisin B inhibits influenza A virus replication by multi-targeting neuraminidase and virus-induced oxidative stress
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topic_title	RM1-950 Vitisin B inhibits influenza A virus replication by multi-targeting neuraminidase and virus-induced oxidative stress Influenza Vitisin B Vitis vinifera L. Neuraminidase Reactive oxygen species NF-κB
topic	misc RM1-950 misc Influenza misc Vitisin B misc Vitis vinifera L. misc Neuraminidase misc Reactive oxygen species misc NF-κB misc Therapeutics. Pharmacology
topic_unstemmed	misc RM1-950 misc Influenza misc Vitisin B misc Vitis vinifera L. misc Neuraminidase misc Reactive oxygen species misc NF-κB misc Therapeutics. Pharmacology
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title	Vitisin B inhibits influenza A virus replication by multi-targeting neuraminidase and virus-induced oxidative stress
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title_full	Vitisin B inhibits influenza A virus replication by multi-targeting neuraminidase and virus-induced oxidative stress
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title_sort	vitisin b inhibits influenza a virus replication by multi-targeting neuraminidase and virus-induced oxidative stress
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title_auth	Vitisin B inhibits influenza A virus replication by multi-targeting neuraminidase and virus-induced oxidative stress
abstract	The development of drug-resistant influenza and new pathogenic virus strains underscores the need for antiviral therapeutics. Currently, neuraminidase (NA) inhibitors are commonly used antiviral drugs approved by the US Food and Drug Administration (FDA) for the prevention and treatment of influenza. Here, we show that vitisin B (VB) inhibits NA activity and suppresses H1N1 viral replication in MDCK and A549 cells. Reactive oxygen species (ROS), which frequently occur during viral infection, increase virus replication by activating the NF-κB signaling pathway, downmodulating glucose-6-phosphate dehydrogenase (G6PD) expression, and decreasing the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant response activity. VB decreased virus-induced ROS generation by increasing G6PD expression and Nrf2 activity, and inhibiting NF-κB translocation to the nucleus through IKK dephosphorylation. In addition, VB reduced body weight loss, increased survival, decreased viral replication and the inflammatory response in the lungs of influenza A virus (IAV)-infected mice. Taken together, our results indicate that VB is a promising therapeutic candidate against IAV infection, complements existing drug limitations targeting viral NA. It modulated the intracellular ROS by G6PD, Nrf2 antioxidant response pathway, and NF-κB signaling pathway. These results demonstrate the feasibility of a multi-targeting drug strategy, providing new approaches for drug discovery against IAV infection.
abstractGer	The development of drug-resistant influenza and new pathogenic virus strains underscores the need for antiviral therapeutics. Currently, neuraminidase (NA) inhibitors are commonly used antiviral drugs approved by the US Food and Drug Administration (FDA) for the prevention and treatment of influenza. Here, we show that vitisin B (VB) inhibits NA activity and suppresses H1N1 viral replication in MDCK and A549 cells. Reactive oxygen species (ROS), which frequently occur during viral infection, increase virus replication by activating the NF-κB signaling pathway, downmodulating glucose-6-phosphate dehydrogenase (G6PD) expression, and decreasing the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant response activity. VB decreased virus-induced ROS generation by increasing G6PD expression and Nrf2 activity, and inhibiting NF-κB translocation to the nucleus through IKK dephosphorylation. In addition, VB reduced body weight loss, increased survival, decreased viral replication and the inflammatory response in the lungs of influenza A virus (IAV)-infected mice. Taken together, our results indicate that VB is a promising therapeutic candidate against IAV infection, complements existing drug limitations targeting viral NA. It modulated the intracellular ROS by G6PD, Nrf2 antioxidant response pathway, and NF-κB signaling pathway. These results demonstrate the feasibility of a multi-targeting drug strategy, providing new approaches for drug discovery against IAV infection.
abstract_unstemmed	The development of drug-resistant influenza and new pathogenic virus strains underscores the need for antiviral therapeutics. Currently, neuraminidase (NA) inhibitors are commonly used antiviral drugs approved by the US Food and Drug Administration (FDA) for the prevention and treatment of influenza. Here, we show that vitisin B (VB) inhibits NA activity and suppresses H1N1 viral replication in MDCK and A549 cells. Reactive oxygen species (ROS), which frequently occur during viral infection, increase virus replication by activating the NF-κB signaling pathway, downmodulating glucose-6-phosphate dehydrogenase (G6PD) expression, and decreasing the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant response activity. VB decreased virus-induced ROS generation by increasing G6PD expression and Nrf2 activity, and inhibiting NF-κB translocation to the nucleus through IKK dephosphorylation. In addition, VB reduced body weight loss, increased survival, decreased viral replication and the inflammatory response in the lungs of influenza A virus (IAV)-infected mice. Taken together, our results indicate that VB is a promising therapeutic candidate against IAV infection, complements existing drug limitations targeting viral NA. It modulated the intracellular ROS by G6PD, Nrf2 antioxidant response pathway, and NF-κB signaling pathway. These results demonstrate the feasibility of a multi-targeting drug strategy, providing new approaches for drug discovery against IAV infection.
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title_short	Vitisin B inhibits influenza A virus replication by multi-targeting neuraminidase and virus-induced oxidative stress
url	https://doi.org/10.1016/j.apsb.2022.07.001 https://doaj.org/article/7c046e5532d14f3ca54a8fdd2001d638 http://www.sciencedirect.com/science/article/pii/S2211383522003124 https://doaj.org/toc/2211-3835
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up_date	2024-07-03T18:10:40.246Z
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Taken together, our results indicate that VB is a promising therapeutic candidate against IAV infection, complements existing drug limitations targeting viral NA. It modulated the intracellular ROS by G6PD, Nrf2 antioxidant response pathway, and NF-κB signaling pathway. 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Vitisin B inhibits influenza A virus replication by multi-targeting neuraminidase and virus-induced oxidative stress

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