Silver Nanoparticle Based Codelivery of Oseltamivir to Inhibit the Activity of the H1N1 Influenza Virus through ROS-Mediated Signaling Pathways

2016 ◽  
Vol 8 (37) ◽  
pp. 24385-24393 ◽  
Author(s):  
Yinghua Li ◽  
Zhengfang Lin ◽  
Mingqi Zhao ◽  
Tiantian Xu ◽  
Changbing Wang ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Signaling Pathways ◽  
Silver Nanoparticle ◽  
H1n1 Influenza ◽  
H1n1 Influenza Virus

scholarly journals Inhibition of H1N1 influenza virus by selenium nanoparticles loaded with zanamivir through p38 and JNK signaling pathways

RSC Advances ◽  
2017 ◽  
Vol 7 (56) ◽  
pp. 35290-35296 ◽  
Author(s):  
Zhengfang Lin ◽  
Yinghua Li ◽  
Min Guo ◽  
Misi Xiao ◽  
Changbing Wang ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
Signaling Pathways ◽  
Clinical Application ◽  
Influenza Virus Infection ◽  
Aqueous Solubility ◽  
H1n1 Influenza ◽  
Solubility Limit ◽  
H1n1 Influenza Virus ◽  
Jnk Signaling

Zanamivir is an effective drug for influenza virus infection, but strong molecular polarity and aqueous solubility limit its clinical application.

scholarly journals The Inhibition of H1N1 influenza virus-induced apoptosis by functionalized Selenium nanoparticles with β-Thujaplicin through ROS-mediated P53 and AKT signaling pathways

2020 ◽  
Author(s):  
Changbing Wang ◽  
Mingqi Zhao ◽  
Zhengfang Lin ◽  
Min Guo ◽  
Tiantian Xu ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Signaling Pathways ◽  
Mdck Cells ◽  
Biological Activities ◽  
Chromatin Condensation ◽  
H1n1 Influenza ◽  
Selenium Nanoparticles ◽  
H1n1 Influenza Virus ◽  
Biomedical Intervention ◽  
Mechanistic Investigation

Abstract β-Thujaplicin possess a variety of biological activities. The use of modified biological nanoparticles (NPs) to develop novel anti-influenza drugs has increased in recent years. Selenium nanoparticles (SeNPs) with antiviral has attracted increasing attention for biomedical intervention. Functionalized SeNPs by β-Thujaplicin (Se@TP) surface modified with superior antiviral were synthesized in this study. β-Thujaplicin decoration of SeNPs obviously inhibited H1N1 infection and were less toxicity. Se@TP could inhibit H1N1 from infecting Madin Darby Canine Kidney (MDCK) cells and block chromatin condensation and DNA fragmentation. Se@TP obviously prevented MDCK cells from generating reactive oxygen species (ROS). Furthermore, Se@TP prevent lung injury in H1N1 infected mice through eosin staining and hematoxylin in vivo . Additionally, when treated with Se@TP, the DNA damage of lung tissues reduced substantially by TUNEL-DAPI test. Mechanistic investigation revealed that Se@TP inhibited H1N1 influenza virus from infecting MDCK cells through induction of apoptosis via suppression AKT and p53 signaling pathways through Immunohistochemical assay. Our results suggest that β-Thujaplicin modified SeNPs as carriers is an efficient way to achieve antiviral pharmaceutical candidate for H1N1 influenza.

Inhibition of H1N1 influenza virus-induced apoptosis by selenium nanoparticles functionalized with arbidol through ROS-mediated signaling pathways

2019 ◽  
Vol 7 (27) ◽  
pp. 4252-4262 ◽  
Author(s):  
Yinghua Li ◽  
Zhengfang Lin ◽  
Guifang Gong ◽  
Min Guo ◽  
Tiantian Xu ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Signaling Pathways ◽  
Clinical Application ◽  
Antiviral Agent ◽  
H1n1 Influenza ◽  
Selenium Nanoparticles ◽  
Drug Resistant ◽  
H1n1 Influenza Virus ◽  
Induced Apoptosis

As an effective antiviral agent, the clinical application of arbidol is limited by the appearance of drug-resistant viruses.

scholarly journals Sequential Seasonal H1N1 Influenza Virus Infections Protect Ferrets against Novel 2009 H1N1 Influenza Virus

2012 ◽  
Vol 87 (3) ◽  
pp. 1400-1410 ◽  
Author(s):  
Donald M. Carter ◽  
Chalise E. Bloom ◽  
Eduardo J. M. Nascimento ◽  
Ernesto T. A. Marques ◽  
Jodi K. Craigo ◽  
...  
Keyword(s):  
Influenza Virus ◽  
H1n1 Influenza ◽  
Cross Reactivity ◽  
Influenza Viruses ◽  
The Novel ◽  
Virus Infections ◽  
H1n1 Influenza Virus ◽  
Virus Shedding ◽  
2009 H1n1 ◽  
Novel H1n1 Influenza

ABSTRACTIndividuals <60 years of age had the lowest incidence of infection, with ∼25% of these people having preexisting, cross-reactive antibodies to novel 2009 H1N1 influenza. Many people >60 years old also had preexisting antibodies to novel H1N1. These observations are puzzling because the seasonal H1N1 viruses circulating during the last 60 years were not antigenically similar to novel H1N1. We therefore hypothesized that a sequence of exposures to antigenically different seasonal H1N1 viruses can elicit an antibody response that protects against novel 2009 H1N1. Ferrets were preinfected with seasonal H1N1 viruses and assessed for cross-reactive antibodies to novel H1N1. Serum from infected ferrets was assayed for cross-reactivity to both seasonal and novel 2009 H1N1 strains. These results were compared to those of ferrets that were sequentially infected with H1N1 viruses isolated prior to 1957 or more-recently isolated viruses. Following seroconversion, ferrets were challenged with novel H1N1 influenza virus and assessed for viral titers in the nasal wash, morbidity, and mortality. There was no hemagglutination inhibition (HAI) cross-reactivity in ferrets infected with any single seasonal H1N1 influenza viruses, with limited protection to challenge. However, sequential H1N1 influenza infections reduced the incidence of disease and elicited cross-reactive antibodies to novel H1N1 isolates. The amount and duration of virus shedding and the frequency of transmission following novel H1N1 challenge were reduced. Exposure to multiple seasonal H1N1 influenza viruses, and not to any single H1N1 influenza virus, elicits a breadth of antibodies that neutralize novel H1N1 even though the host was never exposed to the novel H1N1 influenza viruses.

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