Effects of polyphenol compounds on influenza A virus replication and definition of their mechanism of action

Fioravanti, Rossella; Celestino, Ignacio; Costi, Roberta; Crucitti, Giuliana Cuzzucoli; Pescatori, Luca; Mattiello, Leonardo; Novellino, Ettore; Checconi, Paola; Palamara, Anna Teresa; Nencioni, Lucia; Santo, Roberto Di

doi:10.1016/j.bmc.2012.05.062

Cited by 39 publications

(30 citation statements)

References 57 publications

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“…This latter facilitates nuclear export of the viral ribonucleoprotein (vRNP) complexes, through phosphorylation of the viral nucleoprotein (NP), an event that is essential for the protein’s translocation from the nucleus to the cytoplasm [41]. The nuclear-cytoplasmic traffic of vRNP is blocked by the natural phenol, resveratrol, or its synthetic analogues, through inhibition of the protein kinase C (PKC) phosphorylation and its dependent pathways, c-Jun NH 2 -terminal kinase (JNK) and p38 MAPK, leading to a significant reduction in influenza virus replication [42,43]. Cadmium is known to activate PKC, which results in enhanced phosphorylation of various transcription factors and activation of target gene expression [30].…”

Section: Resultsmentioning

confidence: 99%

The Environmental Pollutant Cadmium Promotes Influenza Virus Replication in MDCK Cells by Altering Their Redox State

Checconi

Sgarbanti²,

Celestino

et al. 2013

IJMS

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Cadmium (Cd) is a toxic heavy metal that is considered an environmental contaminant. Several sources of human exposure to Cd, including employment in primary metal industries, production of certain batteries, foods, soil and cigarette smoke, are known. Its inhalation has been related to different respiratory diseases and toxic effects, among which alterations of the physiological redox state in individuals exposed to the metal have been described. Host-cell redox changes characteristic of oxidative stress facilitate the progression of viral infection through different mechanisms. In this paper, we have demonstrated that pre-treatment with CdCl2 of MDCK cells increased influenza virus replication in a dose-dependent manner. This phenomenon was related to increased viral protein expression (about 40% compared with untreated cells). The concentration of CdCl2, able to raise the virus titer, also induced oxidative stress. The addition of two antioxidants, a glutathione (GSH) derivative or the GSH precursor, N-acetyl-l-cysteine, to Cd pre-treated and infected cells restored the intracellular redox state and significantly inhibited viral replication. In conclusion, our data demonstrate that Cd-induced oxidative stress directly increases the ability of influenza virus to replicate in the host-cell, thus suggesting that exposure to heavy metals, such as this, could be a risk factor for individuals exposed to a greater extent to the contaminant, resulting in increased severity of virus-induced respiratory diseases.

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Section: Resultsmentioning

confidence: 99%

The Environmental Pollutant Cadmium Promotes Influenza Virus Replication in MDCK Cells by Altering Their Redox State

Checconi

Sgarbanti²,

Celestino

et al. 2013

IJMS

Self Cite

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“…Resveratrol significantly reduces influenza virus replication by inhibiting protein kinase C (PKC) phosphorylation and its dependent pathways, JNK and p38 mitogen-activated protein kinase (MAPK) (45). Resveratrol also reduces the inflammation and AHR caused by enhanced IFN-␥ after RSV infection (27).…”

Section: Discussionmentioning

confidence: 99%

Resveratrol Inhibits the TRIF-Dependent Pathway by Upregulating Sterile Alpha and Armadillo Motif Protein, Contributing to Anti-Inflammatory Effects after Respiratory Syncytial Virus Infection

Liu

Zang

Zhou

et al. 2014

J Virol

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Respiratory syncytial virus (RSV) is the most important cause of lower respiratory tract infection in young children ELISA). SARM expression was reduced and TRIF expression was increased after infection with RSV. Resveratrol increased SARM expression and decreased TRIF expression after RSV infection. SARM knockdown in resveratrol-treated mice enhanced gamma interferon production, RSV-induced airway inflammation, and airway hyperresponsiveness (AHR). Resveratrol decreased TRIF expression and prevented the RSV-mediated reduction of SARM expression. Resveratrol-mediated inhibition of the TRIF-dependent pathway may be dependent on SARM expression. IMPORTANCEOur study provides insights into the regulation of innate immunity in response to RSV infection. The results suggest that resveratrol-mediated alterations in SARM have therapeutic potential against RSV immunopathology caused by deregulation of the TLR-mediated immune response. Ultimately, improved insight into the complex interplay between TLR adaptor proteins and the occurrence of severe RSV infection might lead to novel therapeutic treatment strategies, such as TLR adjuvants.

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“…In laboratory previous work, we identified the antiviral activities of 18 kinds of traditional Chinese medicines against DEV and discovered that the crude extract of Rhizoma polygoni cuspidate can inhibit the infection of DEV in DEFs [13]. Resveratrol, one of the main biologically active ingredients of Rhizoma polygoni cuspidate that has been proven to be an efficient agent on several kinds of virus [25],[26],[27],[28],[29],[30],[31],[32],[33],[34], was investigated for its antiviral activity against DEV in this paper. The results indicated that resveratrol effectively reduce the virus titer of DEV in DEFs and protected DEFs from DEV induced cell death in a dose-dependent manner (Fig.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory Effect of Resveratrol against Duck Enteritis Virus In Vitro

Yin

et al. 2013

PLoS ONE

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Duck viral enteritis (DVE) is an acute, contagious herpesvirus infection of ducks, geese, and swans of all ages and species. This disease has been responsible for significant economic losses in domestic and wild waterfowl as a result of mortality, and decreased egg production. Resveratrol is a naturally occurring phytoalexin in specific plants and exhibits inhibitory activity against many kinds of virus. In this paper, resveratrol was found to inhibit duck enteritis virus (DEV) replication in a dose-dependent manner, with a 50% inhibition concentration of 3.85 μg/mL. The inhibition in virus multiplication in the presence of resveratrol was not attributed to direct inactivation or inhibition of virus attachment to the host cells, but to the inhibition of viral multiplication in host cells. The assay of the time of addition limited the drug effect during the first 8 h of infection. This conclusion was supported by the ultrastructure images of the early stage of DEV infection, which showed that the replication of virus nucleic acid and the formation of the capsid in the cell nucleus were suppressed. In the indirect immunofluorescence assay, proteins expression in DEV infected duck embryo fibroblasts (DEFs) within 24 h post-infection (p.i.) was also effectively suppressed by resveratrol. In summary, the resveratrol has a good activity against DEV infection in vitro, which could be attributed to that fact that several essential immediate early viral proteins for virus replication were impacted by resveratrol.

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Effects of polyphenol compounds on influenza A virus replication and definition of their mechanism of action

Cited by 39 publications

References 57 publications

The Environmental Pollutant Cadmium Promotes Influenza Virus Replication in MDCK Cells by Altering Their Redox State

The Environmental Pollutant Cadmium Promotes Influenza Virus Replication in MDCK Cells by Altering Their Redox State

Resveratrol Inhibits the TRIF-Dependent Pathway by Upregulating Sterile Alpha and Armadillo Motif Protein, Contributing to Anti-Inflammatory Effects after Respiratory Syncytial Virus Infection

Inhibitory Effect of Resveratrol against Duck Enteritis Virus In Vitro

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