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In vitro antiviral activity of fluoroquinolones against African swine fever virus.
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African swine fever (ASF) is a viral swine disease against which neither an effective vaccine nor a treatment is available. The antiviral effect of thirty fluoroquinolones on the infectivity of African swine fever virus (ASFV) was screened in vitro. There was a severe reduction of the cytopathic
African swine fever virus blocks the host cell antiviral inflammatory response through a direct inhibition of PKC-theta-mediated p300 transactivation.
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During a viral infection, reprogramming of the host cell gene expression pattern is required to establish an adequate antiviral response. The transcriptional coactivators p300 and CREB binding protein (CBP) play a central role in this regulation by promoting the assembly of transcription enhancer
Inhibition of Heme Oxygenase-1 enhances hyperthermia-induced autophagy and antiviral effect.
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Hyperthermia has been clinically utilized as an adjuvant therapy in the treatment of cervical carcinoma. However, thermotolerance induced by heme oxygenase-1 (HO-1), a stress-inducible cytoprotective protein, limits the efficacy of hyperthermic therapy, for which the exact mechanism remains unknown.
Classical swine fever virus interferes with cellular antiviral defense: evidence for a novel function of N(pro).
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Classical swine fever virus (CSFV) replicates efficiently in cell lines and monocytic cells, including macrophages (MPhi), without causing a cytopathic effect or inducing interferon (IFN) secretion. In the present study, the capacity of CSFV to interfere with cellular antiviral activity was
Inhibition of sandfly fever Sicilian virus (Phlebovirus) replication in vitro by antiviral compounds.
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Sandfly fever Sicilian virus (SFSV) was used in our laboratory to screen antiviral substances active toward viruses of the Bunyaviridae family. Antiviral activity was estimated by the reduction of the cytopathic effect of SFSV on infected Vero cells. Cytotoxicity was evaluated by determining the
Antiviral drug discovery and development for Mayaro Fever - What do we have so far?
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Tropical infectious diseases cause millions of deaths every year in developing countries with about half of the world population living at risk. Mayaro virus (MAYV) is an emerging arbovirus that causes Mayaro fever, which is characterized by fever, headache, diarrhea, arthralgia and rash. These
Comparison of antiviral activity of recombinant and natural interferons against crimean-congo hemorrhagic Fever virus.
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As a first line of defence against a virus infection, mammalian cells elicit an innate immune response, characterized by secretion of type I interferons (IFN) and up-regulation of interferon stimulated genes (ISGs). We have previously included Crimean Congo Hemorrhagic Fever Virus (CCHFV) in the
Intra-host variation structure of classical swine fever virus NS5B in relation to antiviral therapy.
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Classical swine fever (CSF) is one of most important diseases of the Suidea with severe social economic consequences in case of outbreaks. Antivirals have been demonstrated, in recent publications, to be an interesting alternative method of fighting the disease. However, classical swine fever virus
A simple assay for determining antiviral activity against Crimean-Congo hemorrhagic fever virus.
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Crimean-Congo hemorrhagic fever virus (CCHFV) is a tick-borne virus that is emerging as a significant human pathogen in many regions of the world, including Africa, Asia, and Europe. In this report, we describe a simple screening method for discovering new antiviral compounds directed against CCHFV.
[Antiviral effectiveness of the combined use of amixine and virasole in experimental hemorrhagic fever with renal syndrome in sucking albino mice].
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The antiviral effectiveness of the combined and single use of superlow-dose amixine and virasole on the course of experimental hemorrhagic fever with renal syndrome was studied in sucking albino mice parenterally infected with their virus Hantaan. The co-administration of virasole and amixine was
Delayed Interferon Type 1-Induced Antiviral State Is a Potential Factor for Hemorrhagic Fever With Renal Syndrome Severity.
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Hantaviruses cause hemorrhagic fever with renal syndrome (HFRS) in Europe and Asia. Interferon (IFN) responses play an important role in HFRS pathogenesis and early IFN-β response is delayed by pathogenic hantaviruses. The severity of HFRS caused by Dobrava virus (DOBV) and Puumala virus (PUUV)
The R614E mutation of mouse Mx1 protein contributes to the novel antiviral activity against classical swine fever virus.
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Mx proteins are interferon-induced GTPases that have broad antiviral activity against a wide range of RNA and DNA viruses. We previously demonstrated that porcine Mx1 protein (poMx1) inhibited the replication of classical swine fever virus (CSFV), an economically important Pestivirus, and that mouse
Retrovirus-Based Surrogate Systems for BSL-2 High-Throughput Screening of Antivirals Targeting BSL-3/4 Hemorrhagic Fever-Causing Viruses.
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The majority of viruses causing hemorrhagic fever in humans are Risk Group 3 or 4 pathogens and, therefore, can only be handled in biosafety level 3 or 4 (BSL-3/4) containment laboratories. The restricted number of such laboratories, the substantial financial requirements to maintain them, and
Expression of interferon-induced antiviral genes is delayed in a STAT1 knockout mouse model of Crimean-Congo hemorrhagic fever.
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BACKGROUND
Crimean Congo hemorrhagic fever (CCHF) is a tick-borne hemorrhagic zoonosis associated with high mortality. Pathogenesis studies and the development of vaccines and antivirals against CCHF have been severely hampered by the lack of suitable animal model. We recently developed and
Dengue fever virus and Japanese encephalitis virus synthetic peptides, with motifs to fit HLA class I haplotypes prevalent in human populations in endemic regions, can be used for application to skin Langerhans cells to prime antiviral CD8+ cytotoxic T cells (CTLs)--a novel approach to the protection of humans.
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Flaviviruses were reported to induce CD8+ cytotoxic T cells in infected individuals, indicating that nonapeptides, proteolytic cleavage products of the viral precursor protein, enter the endoplasmic reticulum in infected cells and interact with HLA class I molecules. The assembled HLA class I
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