<sec>
<title>Objectives</title>
<p>Human rhinoviruses (HRVs) are the major cause of the common cold. Currently there is no registered, clinically effective, antiviral chemotherapeutic agent to treat diseases caused by HRVs. In this study, the antiviral activity of dexamethasone (DEX) against HRV1B was examined.</p></sec>
<sec>
<title>Methods</title>
<p>The anti–HRV1B activity of DEX was assessed by sulforhodamine B assay in HeLa cells, and by RT-PCR in the lungs of HRV1B-infected mice. Histological evaluation of HRV1B-infected lungs was performed and a histological score was given. Anti-HRV1B activity of DEX via the glucocorticoid receptor (GCR)-dependent autophagy activation was assessed by blocking with chloroquine diphosphate salt or bafilomycin A1 treatment.</p></sec>
<sec>
<title>Results</title>
<p>In HRV1B-infected HeLa cells, treatment with DEX in a dose-dependent manner, resulted in a cell viability of > 70% indicating that HRV1B viral replication was reduced by DEX treatment. HRV1B infected mice treated with DEX, had evidence of reduced inflammation and a moderate histological score. DEX treatment showed antiviral activity against HRV1B via GCR-dependent autophagy activation.</p></sec>
<sec>
<title>Conclusion</title>
<p>This study demonstrated that DEX treatment showed anti-HRV1B activity via GCR-dependent autophagy activation in HeLa cells and HRV1B infected mice. Further investigation assessing the development of topical formulations may enable the development of improved DEX effectiveness.</p></sec>
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<sec><title>Objectives</title><p>Rhinoviruses (RVs) cause common cold and are associated with exacerbation of chronic inflammatory respiratory diseases. Until now, no clinically effective antiviral chemotherapeutic agents to treat diseases caused by human rhinoviruses (HRVs) have been reported. We assessed the anti-HRV3 activity of sakuranetin isolated from <italic>Sorbus commixta</italic> Hedl. in human epithelioid carcinoma cervix (HeLa) cells, to evaluate its anti-rhinoviral potential in the clinical setting.</p></sec><sec><title>Methods</title><p>Antiviral activity and cytotoxicity as well as the effect of sakuranetin on HRV3-induced cytopathic effects (CPEs) were evaluated using the sulforhodamine B (SRB) method using CPE reduction. The morphology of HRV3-infected cells was studied using a light microscope.</p></sec><sec><title>Results</title><p>Sakuranetin actively inhibited HRV3 replication and exhibited antiviral activity of more than 67% without cytotoxicity in HeLa cells, at 100 μg/mL. Ribavirin showed anti-HRV3 activity similar to that of sakuranetin. Treatment of HRV-infected HeLa cells with sakuranetin visibly reduced CPEs.</p></sec><sec><title>Conclusion</title><p>The inhibition of HRV production by sakuranetin is mainly due to its general antioxidant activity through inhibition of viral adsorption. Therefore, the antiviral activity of sakuranetin should be further investigated to elucidate its mode of action and prevent HRV3-mediated diseases in pathological conditions.</p></sec>
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