tetano
Editor, Senior Moderator
J Ethnopharmacol. 2013 Feb 22. pii: S0378-8741(13)00114-1. doi: 10.1016/j.jep.2013.02.020. [Epub ahead of print]
A polyphenol-rich extract from Chaenomeles sinensis (Chinese quince) inhibits influenza A virus infection by preventing primary transcription in vitro.
Sawai-Kuroda R, Kikuchi S, Shimizu YK, Sasaki Y, Kuroda K, Tanaka T, Yamamoto T, Sakurai K, Shimizu K.
Source
Open Research Center for Genome and Infectious Disease Control, Nihon University School of Medicine, 30-1 Oyaguchikami-chou, Itabashi-ku, Tokyo 173-8610, Japan; Central Laboratory, Lotte Co., Ltd., 3-1-1 Numakage, Minami-ku, Saitama, Saitama 336-8601, Japan. Electronic address: Kuroda_Reiko@lotte.co.jp.
Abstract
ETHNOPHARMACOLOGICAL RELEVANCE:
The fruits of Chaenomeles sinensis Koehne (Chinese quince) are distributed throughout China and Japan. It has traditionally been known to have a therapeutic effect against respiratory symptoms caused by infectious diseases.
AIM OF THE STUDY:
The polyphenol-rich extract, CSD3, from Chaenomeles sinensis has previously been shown to neutralize influenza virus infectivity. The aim of this study was to clarify which step(s) in the replication cycle in vitro were inhibited.
MATERIALS AND METHODS:
We examined cell-binding, hemagglutination and hemolytic activities and infectivity of A/Udorn/72(H3N2) virus after pre-treatment with CSD3. We also investigated the time course of synthesis for viral mRNA, cRNA, and vRNA in Madin-Darby canine kidney epithelial cells (MDCK) cells infected with CSD3-treated virus. Finally, we studied the effect of CSD3-treatment on the ultrastructure of the influenza virion.
RESULTS:
Pre-treatment with CSD3 mildly reduced cell-binding, hemagglutination and hemolytic activities. These activities were reduced by 70% to be equivalent to 30% of the control at 1μg/ml. CSD3 severely reduced infectivity to 1% of the control at 1μg/ml. Primary transcription in MDCK cells infected with CSD3 (1μg/ml)-treated virus was decreased to about 1% of that in cells infected with mock-treated virus. Synthesis of viral cRNA, vRNA and secondary mRNA was also severely decreased. Electron microscopy revealed that the integrity of the virus envelope was damaged by CSD3 and was permeable to uranyl acetate.
CONCLUSIONS:
The main target step(s) of CSD3 in the replication cycle is after cell-binding but before or at primary transcription. Involvement of the increased permeability of virus envelope as the inhibition mechanism was proposed. CSD3 could be useful in preventing influenza virus infection, and be employed as a lozenge or mouthwash for daily use.
Copyright ? 2013. Published by Elsevier Ireland Ltd.
PMID:
23439031
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/23439031
A polyphenol-rich extract from Chaenomeles sinensis (Chinese quince) inhibits influenza A virus infection by preventing primary transcription in vitro.
Sawai-Kuroda R, Kikuchi S, Shimizu YK, Sasaki Y, Kuroda K, Tanaka T, Yamamoto T, Sakurai K, Shimizu K.
Source
Open Research Center for Genome and Infectious Disease Control, Nihon University School of Medicine, 30-1 Oyaguchikami-chou, Itabashi-ku, Tokyo 173-8610, Japan; Central Laboratory, Lotte Co., Ltd., 3-1-1 Numakage, Minami-ku, Saitama, Saitama 336-8601, Japan. Electronic address: Kuroda_Reiko@lotte.co.jp.
Abstract
ETHNOPHARMACOLOGICAL RELEVANCE:
The fruits of Chaenomeles sinensis Koehne (Chinese quince) are distributed throughout China and Japan. It has traditionally been known to have a therapeutic effect against respiratory symptoms caused by infectious diseases.
AIM OF THE STUDY:
The polyphenol-rich extract, CSD3, from Chaenomeles sinensis has previously been shown to neutralize influenza virus infectivity. The aim of this study was to clarify which step(s) in the replication cycle in vitro were inhibited.
MATERIALS AND METHODS:
We examined cell-binding, hemagglutination and hemolytic activities and infectivity of A/Udorn/72(H3N2) virus after pre-treatment with CSD3. We also investigated the time course of synthesis for viral mRNA, cRNA, and vRNA in Madin-Darby canine kidney epithelial cells (MDCK) cells infected with CSD3-treated virus. Finally, we studied the effect of CSD3-treatment on the ultrastructure of the influenza virion.
RESULTS:
Pre-treatment with CSD3 mildly reduced cell-binding, hemagglutination and hemolytic activities. These activities were reduced by 70% to be equivalent to 30% of the control at 1μg/ml. CSD3 severely reduced infectivity to 1% of the control at 1μg/ml. Primary transcription in MDCK cells infected with CSD3 (1μg/ml)-treated virus was decreased to about 1% of that in cells infected with mock-treated virus. Synthesis of viral cRNA, vRNA and secondary mRNA was also severely decreased. Electron microscopy revealed that the integrity of the virus envelope was damaged by CSD3 and was permeable to uranyl acetate.
CONCLUSIONS:
The main target step(s) of CSD3 in the replication cycle is after cell-binding but before or at primary transcription. Involvement of the increased permeability of virus envelope as the inhibition mechanism was proposed. CSD3 could be useful in preventing influenza virus infection, and be employed as a lozenge or mouthwash for daily use.
Copyright ? 2013. Published by Elsevier Ireland Ltd.
PMID:
23439031
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/23439031