The impact of non-pharmaceutical interventions for 2009 H1N1 influenza on travel intentions: A model of goal-directed behavior.

The impact of non-pharmaceutical interventions for 2009 H1N1 influenza on travel intentions: A model of goal-directed behavior.

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Theoretically, in the tourism context this study introduced a new concept of non-pharmaceutical intervention (NPI) for influenza, and tested the impact of NPI on the behavioral intention of potential international tourists. This study also extended the model of goal-directed behavior (MGB) by incorporating the new concepts of NPI, and the perception of 2009 H1N1.

The model found that desire, perceived behavioral control, frequency of past behavior, and non-pharmaceutical interventions predicted tourists’ intention but perceptions of 2009 H1N1 had nil effect on desire and intention. Personal non-pharmaceutical interventions were theorized as adaptive behavior of tourists intending to travel during a pandemic which should be supported by tourism operators on a system-wide basis.

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Practically, this study dealt with the issue of influenza 2009 H1N1 with the study findings and implications providing government agencies, tourism marketers, policy-makers, transport systems, and hospitality services with important suggestions for NPI and international tourism during pandemics.

The impact of non-pharmaceutical interventions for 2009 H1N1 influenza on travel intentions: A model of goal-directed behavior.
The impact of non-pharmaceutical interventions for 2009 H1N1 influenza on travel intentions: A model of goal-directed behavior.

Antiviral Activity of Fritillaria thunbergii extract against Human Influenza Virus H1N1 (PR8) in vitro, in ovo and in vivo.

.Influenza viruses cause respiratory diseases in humans and animals with high morbidity and mortality rates. Conventional anti-influenza drugs are reported to exert side-effects and newly emerging viral strains tend to develop resistance to these commonly used agents. Fritillaria thunbergii (FT) is traditionally used as an expectorant for controlling airway inflammatory disorders.

Here, we evaluated the therapeutic effects of FT extracts against influenza virus type A (H1N1) infection in vitro, in ovo, and in vivo. In the post-treatment assay, FT extracts showed high CC50 (7500 µg/ml) indicating low toxicity and exerted moderate antiviral effects, compared to Oseltamivir (SI 50.6 vs. 222) in vitro. Antiviral activity tests in ovo revealed strong inhibitory effects of both FT extract and Oseltamivir against H1N1 replication in embryonated eggs.

Notably, at a treatment concentration of 150 mg/kg, only half the group administered Oseltamivir survived whereas the FT group showed 100% survival, clearly supporting low toxicity of FT extracts. Consistent with these findings, FT-administered mice showed a higher survival rate with lower body weight reduction relative to the Oseltamivir group upon treatment 24 h after viral infection.

Our collective results suggest that FT extracts exert antiviral effects against influenza H1N1 virus without inducing toxicity in vitro, in ovo and in vivo, supporting its potential utility as a novel candidate therapeutic drug or supplement against influenza.

MicroRNA-132-3p suppress type I IFN response through targeting IRF1 to facilitate H1N1 influenza A virus infection.

Increasing evidence has indicated that microRNAs (miRNAs) have essential roles in innate immune responses to various viral infections; however, the role of miRNAs in H1N1 influenza A virus (IAV) infection is still unclear. The present study aimed to elucidate the role and mechanism of miRNAs in IAV replication in vitro. Using a microarray assay, we analyzed the expression profiles of miRNAs in peripheral blood from IAV patients. It was found that miR-132-3p was significantly upregulated in peripheral blood samples from IAV patients. It was also observed that IAV infection upregulated the expression of miR-132-3p in a dose and time dependent manner. Subsequently, we investigated miR-132-3p function and found that upregulation of miR-132-3p promoted IAV replication, whereas knockdown of miR-132-3p repressed replication.

Meanwhile, overexpression of miR-132-3p could inhibit IAV triggered INF-α and INF-β production and IFN-stimulated gene (ISG) expression , including myxovirus protein A (MxA), 2´, 5´-oligoadenylate synthetases (OAS), and double stranded RNA-dependent protein kinase (PKR), while inhibition of miR-132-3p enhanced IAV triggered these effects. Of note, interferon regulatory factor 1 (IRF1), a well-known regulator of the type I IFN response, was identified as a direct target of miR-132-3p during HIN1 IAV infection.

Furthermore, knockdown of IRF1 by si-IRF1 reversed the promoting effects of miR-132-3p inhibition on type I IFN response. Taken together, upregulation of miR-132-3p promotes IAV replication by suppressing type I IFN response through its target gene IRF1, suggesting that miR-132-3p could represent a novel potential therapeutic target of IAV treatment.

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