Biomol Ther  
Antiviral and Anti-Inflammatory Activities of Pochonin D, a Heat Shock Protein 90 Inhibitor, against Rhinovirus Infection
Jae-Hyoung Song1,†, Aeri Shim1,†, Yeon-Jeong Kim2, Jae-Hee Ahn1, Bo-Eun Kwon1, Thuy Trang Pham1, Jongkook Lee1, Sun-Young Chang3 and Hyun-Jeong Ko1,*
1College of Pharmacy, Kangwon National University, Chuncheon 24341,
2College of Pharmacy, Inje University, Gimhae 50834,
3College of Pharmacy, Ajou University, Suwon 16499, Republic of Korea
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The first two authors contributed equally to this work.
Received: November 23, 2017; Revised: January 8, 2018; Accepted: February 1, 2018; Published online: May 2, 2018.
© The Korean Society of Applied Pharmacology. All rights reserved.

Human rhinoviruses (HRV) are one of the major causes of common cold in humans and are also associated with acute asthma and bronchial illness. Heat-shock protein 90 (Hsp90), a molecular chaperone, is an important host factor for the replication of single-strand RNA viruses. In the current study, we examined the effect of the Hsp90 inhibitor pochonin D, in vitro and in vivo, using a murine model of human rhinovirus type 1B (HRV1B) infection. Our data suggested that Hsp90 inhibition significantly reduced the inflammatory cytokine production and lung damage caused by HRV1B infection. The viral titer was significantly lowered in HRV1B-infected lungs and in Hela cells upon treatment with pochonin D. Infiltration of innate immune cells including granulocytes and monocytes was also reduced in the bronchoalveolar lavage (BAL) by pochonin D treatment after HRV1B infection. Histological analysis of the lung and respiratory tract showed that pochonin D protected the mice from HRV1B infection. Collectively, our results suggest that the Hsp90 inhibitor, pochonin D, could be an attractive antiviral therapeutic for treating HRV infection.
Keywords: Rrhinovirus, Antiviral activity, Pochonin D, Heat-shock protein 90, Anti-inflammatory

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