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      The Antiviral Effect of Baicalin on Enterovirus 71 In Vitro

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          Abstract

          Baicalin is a flavonoid compound extracted from Scutellaria roots that has been reported to possess antibacterial, anti-inflammatory, and antiviral activities. However, the antiviral effect of baicalin on enterovirus 71 (EV71) is still unknown. In this study, we found that baicalin showed inhibitory activity on EV71 infection and was independent of direct virucidal or prophylactic effect and inhibitory viral absorption. The expressions of EV71/3D mRNA and polymerase were significantly blocked by baicalin treatment at early stages of EV71 infection. In addition, baicalin could decrease the expressions of FasL and caspase-3, as well as inhibit the apoptosis of EV71-infected human embryonal rhabdomyosarcoma (RD) cells. Altogether, these results indicate that baicalin exhibits potent antiviral effect on EV71 infection, probably through inhibiting EV71/3D polymerase expression and Fas/FasL signaling pathways.

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          Most cited references43

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          NF-kappaB signaling differentially regulates influenza virus RNA synthesis.

          The NF-kappaB signaling pathway has previously been shown to be required for efficient influenza A virus replication, although the molecular mechanism is not well understood. In this study, we identified a specific step of the influenza virus life cycle that is influenced by NF-kappaB signaling by using two known NF-kappaB inhibitors and a variety of influenza virus-specific assays. The results of time course experiments suggest that the NF-kappaB inhibitors Bay11-7082 and ammonium pyrrolidinedithiocarbamate inhibited an early postentry step of viral infection, but they did not appear to affect the nucleocytoplasmic trafficking of the viral ribonucleoprotein complex. Instead, we found that the levels of influenza virus genomic RNA (vRNA), but not the corresponding cRNA or mRNA, were specifically reduced by the inhibitors in virus-infected cells, indicating that NF-kappaB signaling is intimately involved in the vRNA synthesis. Furthermore, we showed that the NF-kappaB inhibitors specifically diminished influenza virus RNA transcription from the cRNA promoter but not from the vRNA promoter in a reporter assay, a result which is consistent with data obtained from virus-infected cells. The overexpression of the p65 NF-kappaB molecule could not only eliminate the inhibition but also activate influenza virus RNA transcription from the cRNA promoter. Finally, using p65-specific small interfering RNA, we have shown that p65 knockdown reduced the levels of influenza virus replication and vRNA synthesis. In summary, we have provided evidence showing, for the first time, that the NF-kappaB host signaling pathway can differentially regulate influenza virus RNA synthesis, which may also offer some new perspectives into understanding the host regulation of RNA synthesis by other RNA viruses.
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            Flavonoid baicalin inhibits HIV-1 infection at the level of viral entry.

            Baicalin (BA) is a flavonoid compound purified from medicinal plant Scutellaria baicalensis Georgi and has been shown to possess anti-inflammatory and anti-HIV-1 activities. In an effort to elucidate the mechanism of the anti-inflammatory effect of BA, we recently found that this flavonoid compound was able to form complexes with selected chemokines and attenuated their capacity to bind and activate receptors on the cell surface. These observations prompted us to investigate whether BA could inhibit HIV-1 infection by interfering with viral entry, a process known to involve interaction between HIV-1 envelope proteins and the cellular CD4 and chemokine receptors. We found that BA at the noncytotoxic concentrations, inhibited both T cell tropic (X4) and monocyte tropic (R5) HIV-1 Env protein mediated fusion with cells expressing CD4/CXCR4 or CD4/CCR5. Furthermore, presence of BA at the initial stage of HIV-1 viral adsorption blocked the replication of HIV-1 early strong stop DNA in cells. Since BA did not inhibit binding of HIV-1 gp120 to CD4, we propose that BA may interfere with the interaction of HIV-1 Env with chemokine coreceptors and block HIV-1 entry of target cells. Therefore, BA can be used as a basis for developing novel anti-HIV-1 agents.
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              Cis -acting RNA elements in human and animal plus-strand RNA viruses

              The RNA genomes of plus-strand RNA viruses have the ability to form secondary and higher-order structures that contribute to their stability and to their participation in inter- and intramolecular interactions. Those structures that are functionally important are called cis-acting RNA elements because their functions cannot be complemented in trans. They can be involved not only in RNA/RNA interactions but also in binding of viral and cellular proteins during the complex processes of translation, RNA replication and encapsidation. Most viral cis-acting RNA elements are located in the highly structured 5′- and 3′-nontranslated regions of the genomes but sometimes they also extend into the adjacent coding sequences. In addition, some cis-acting RNA elements are embedded within the coding sequences far away from the genomic ends. Although the functional importance of many of these structures has been confirmed by genetic and biochemical analyses, their precise roles are not yet fully understood. In this review we have summarized what is known about cis-acting RNA elements in nine families of human and animal plus-strand RNA viruses with an emphasis on the most thoroughly characterized virus families, the Picornaviridae and Flaviviridae.
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                Author and article information

                Contributors
                Role: Academic Editor
                Journal
                Viruses
                Viruses
                viruses
                Viruses
                MDPI
                1999-4915
                19 August 2015
                August 2015
                : 7
                : 8
                : 4756-4771
                Affiliations
                [1 ]Department of Clinical Laboratory, Huai’an Hospital Affiliated of Xuzhou Medical College, 62 Huaihai south road, Huai’an, Jiangsu 223300, China; E-Mails: lixiang_suda@ 123456163.com (X.L.); huaianjinyue1999@ 123456163.com (Y.J.); chengjianping2011@ 123456aliyun.com (J.C.); huaianwancb@ 123456163.com (C.W.); huaianqianwh@ 123456163.com (W.Q.); xingfei115@ 123456163.com (F.X.)
                [2 ]Department of Endocrinology, Huai’an First Affliated Hospital of Nanjing Medical University, 6 Beijing west road, Huai’an, Jiangsu 223300, China; E-Mail: liuyy_suda@ 123456163.com
                [3 ]Department of Clinical Laboratory, the Fourth People’s Hospital of Huai’an, 128 Yanan east road, Huai’an, Jiangsu 223300, China; E-Mail: wutt8870@ 123456163.com
                [4 ]Department of Clinical Laboratory, the Third Affiliated Hospital of Soochow University, 185 Juqian street, Changzhou, Jiangsu 213003, China
                Author notes
                [†]

                These author contributed equally to this work.

                [* ]Author to whom correspondence should be addressed; E-Mail: shiweifeng67@ 123456163.com ; Tel.: +86-519-68870895; Fax: +86-519-86621235.
                Article
                viruses-07-02841
                10.3390/v7082841
                4576202
                26295407
                5c318d9d-03ef-4a7b-86a5-2b05a9eb8350
                © 2015 by the authors; licensee MDPI, Basel, Switzerland.

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 19 April 2015
                : 10 August 2015
                Categories
                Article

                Microbiology & Virology
                baicalin,enterovirus 71,3d polymerase,apoptosis
                Microbiology & Virology
                baicalin, enterovirus 71, 3d polymerase, apoptosis

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