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Berlin Brandenburg

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  • Antiviral Agents
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  • 1
    Language: English
    In: BMC Research Notes, June 23, 2014, Vol.7(1)
    Description: Background Different flavonoids are known to interfere with influenza A virus replication. Recently, we showed that the structurally similar flavonoids baicalein and biochanin A inhibit highly pathogenic avian H5N1 influenza A virus replication by different mechanisms in A549 lung cells. Here, we investigated the effects of both compounds on H5N1-induced reactive oxygen species (ROS) formation and the role of ROS formation during H5N1 replication. Findings Baicalein and biochanin A enhanced H5N1-induced ROS formation in A549 cells and primary human monocyte-derived macrophages. Suppression of ROS formation induced by baicalein and biochanin A using the antioxidant N-acetyl-L-cysteine strongly increased the anti-H5N1 activity of both compounds in A549 cells but not in macrophages. Conclusions These findings emphasise that flavonoids induce complex pharmacological actions some of which may interfere with H5N1 replication while others may support H5N1 replication. A more detailed understanding of these actions and the underlying structure-activity relationships is needed to design agents with optimised anti-H5N1 activity. Keywords: H5N1, Biochanin A, Baicalein, Antiviral, Reactive oxygen species, N-acetyl-L-cysteine
    Keywords: Antiviral Agents -- Research ; Antioxidants (Nutrients) -- Research ; Avian Influenza -- Research ; Cystine ; Avian Influenza Viruses ; Macrophages
    ISSN: 1756-0500
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  • 2
    Language: English
    In: Current Molecular Medicine, March 2009, Vol.9(2), pp.131-151
    Description: Highly pathogenic H5N1 avian influenza virus can infect humans and is currently the most deadly influenza virus that has crossed the species barrier. As of December 2007, the spread of H5N1 virus from human to human has been rare. Nobody can predict if H5N1 may cause a pandemic. However, the number of human cases is continuously increasing and changes in virulence and epidemiology have been detected. There are specific pathogenic features of H5N1 infection. In contrast to human-adapted influenza A strains, H5N1 preferentially infects cells of the lower respiratory tract and may spread to tissues outside the respiratory tract in humans. Moreover, H5N1 replication is prolonged in target organs and results in higher viral loads and increased tissue damage. These features will have to be considered for therapeutic protocols for H5N1 infection in humans. Rapid genetic and antigenic changes observed in H5N1 virus isolates represent a challenge for the development of vaccines. In the present review, current knowledge about epidemiology, virulence factors and pathology of H5N1 infections in humans are summarised and discussed. Moreover, the possible roles of antiinfluenza drugs in the pandemic situation as well as the development of effective vaccines are subject of this overview.
    Keywords: Pathogenic H5n1 ; Avian Influenza ; Humans ; Of Chickens ; Epidemiology ; Epidemiology
    ISSN: 1566-5240
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  • 3
    Language: English
    In: The Journal of Infectious Diseases, 09/2000, Vol.182(3), pp.643-651
    Description: In fibroblasts, infection with human cytomegalovirus (HCMV) inhibits expression of the extracellular matrix proteins thrombospondin-1 and -2 (TSP-1 and TSP-2). These effects may depend on expression of HCMV immediate-early (IE) genes, which are activated by cellular transcription factor NF-kappaB. The influence of HCMV infection on TSP-1 and TSP-2 expression and the ability of different antiviral drugs to prevent these cellular changes in permissive cultures of human retinal glial cells were observed. Ganciclovir inhibited only HCMV late antigen (LA) expression, whereas antisense oligonucleotide ISIS 2922 and peptide SN50, inhibitors of HCMV IE expression and NF-kappaB activity, respectively, inhibited both IE and LA expression. ISIS 2922 and SN50, but not ganciclovir, prevented down-modulation of TSP-1 and TSP-2. The results showed that HCMV-induced down-modulation of TSP-1 and TSP-2 in retinal glial cells is prevented by inhibition of HCMV IE expression. These findings may be relevant to pathogenesis and treatment of HCMV retinitis.
    Keywords: Antiviral Agents -- Pharmacology ; Cytomegalovirus Retinitis -- Metabolism ; Neuroglia -- Metabolism ; Retina -- Metabolism ; Thrombospondin 1 -- Biosynthesis ; Thrombospondins -- Biosynthesis;
    ISSN: 0022-1899
    E-ISSN: 1537-6613
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  • 4
    Language: English
    In: Phytomedicine: International Journal of Phytotherapy & Phytopharmacology, March 15, 2011, Vol.18(5), p.384(3)
    Description: The Pelargonium sidoides extract EPs[super][registered] 7630 is an approved drug for the treatment of acute bronchitis in Germany. The postulated mechanisms underlying beneficial effects of EPs[super][registered] 7630 in bronchitis patients include immunomodulatory and cytoprotective effects, inhibition of interaction between bacteria and host cells, and increase of cilliary beat frequency on respiratory cells. Here, we investigated the influence of EPs[super][registered] 7630 on replication of a panel of respiratory viruses. Determination of virus-induced cytopathogenic effects and virus titres revealed that EPs[super][registered] 7630 at concentrations up to 100 [micro]g/ml interfered with replication of seasonal influenza A virus strains (H1N1, H3N2), respiratory syncytial virus, human coronavirus, parainfluenza virus, and coxsackie virus but did not affect replication of highly pathogenic avian influenza A virus (H5N1), adenovirus, or rhinovirus. Therefore, antiviral effects may contribute to the beneficial effects exerted by EPs[super][registered] 7630 in acute bronchitis patients.
    Keywords: Influenza -- Drug Therapy ; Influenza -- Research ; Virus Replication -- Research ; Herbal Medicine -- Health Aspects ; Herbal Medicine -- Research ; Geraniums -- Health Aspects ; Geraniums -- Research
    ISSN: 0944-7113
    E-ISSN: 1618095X
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  • 5
    Language: English
    In: Intervirology, 1994, Vol.37(6), pp.307-314
    Description: Effective therapy of human immunodeficiency virus (HIV) infection is mainly based on inhibition of reverse transcriptase by nucleoside analogues such as zidovudine (azidothymidine; AZT), didanosine, and zalcitabine. A major problem associated with long-term AZT therapy is the waning efficacy (‘clinical resistance’) over time. Clinical isolates of HIV-1 with reduced susceptibility to AZT can be recovered from HIV-infected individuals under prolonged treatment. However, the clinical importance of AZT resistance is uncertain. Other factors such as increased virus burden, increased virulence, and AZT toxicity could contribute, singly or in combination, to the loss of therapeutic benefit. Recent observations based on experimental models and clinical trials suggest that cellular mechanisms (‘cellular resistance’) may account for clinical resistance to antiviral agents. In vitro experiments demonstrated that in analogy to antitumoral therapy, the acquisition of multidrug resistance, i.e., resistance of cells to multiple, structurally unrelated chemotherapeutic agents, may play a role in the failure of long-term antiretroviral therapy. The ‘cellular resistance’ may contribute directly to the failure of antiviral therapy by the generation of sub therapeutic levels of antiviral compounds and/or their active forms. Indirectly, such subtherapeutic concentrations of active substances which permit limited replication of virus may represent a selective pressure for emergence and development of a resistant virus population. Hence it is of great importance to investigate the role of cellular factors in ‘clinical resistance’ to AZT and other anti-HIV agents. More detailed knowledge of cellular interactions and antiviral agents could help to improve or develop new strategies for antiviral therapy regimens.
    Keywords: Review Paper ; Cellular Thymidine Kinase ; Viral Resistance Mechanisms ; Reverse Transcriptase ; Multidrug Resistance ; Glycoprotein P ; Biology
    ISSN: 0300-5526
    E-ISSN: 1423-0100
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  • 6
    Language: English
    In: Intervirology, 1997, Vol.40(5-6), pp.357-367
    Description: This review summarizes current strategies for the treatment of human cytomegalovirus (CMV) infection/diseases in high-risk patients such as transplant recipients and AIDS patients. Since the major drugs ganciclovir (Cytovene), foscarnet (Foscavir) and cidofovir (Vistide) are frequently associated with severe side effects and the formation of viral resistance, it should be endeavored to develop better strategies in anti-CMV treatment. Moreover, blocking of the viral replication does not always resolve the manifestations which are often linked with CMV-associated immunopathomechanisms. Thus, the efficacy of the available drugs is also discussed in the light of their ability to modulate inflammatory components of the cell-mediated immune system.
    Keywords: Treatment of Viral Diseases ; Human Cytomegalovirus ; Antiviral Therapy ; New Drugs ; Biology
    ISBN: 9783805567251
    ISBN: 3805567251
    ISSN: 0300-5526
    E-ISSN: 1423-0100
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  • 7
    Language: English
    In: PLoS ONE, May 17, 2011, Vol.6(5), p.e19705
    Description: Glycyrrhizin is known to exert antiviral and anti-inflammatory effects. Here, the effects of an approved parenteral glycyrrhizin preparation (Stronger Neo-Minophafen C) were investigated on highly pathogenic influenza A H5N1 virus replication, H5N1-induced apoptosis, and H5N1-induced pro-inflammatory responses in lung epithelial (A549) cells. Therapeutic glycyrrhizin concentrations substantially inhibited H5N1-induced expression of the pro-inflammatory molecules CXCL10, interleukin 6, CCL2, and CCL5 (effective glycyrrhizin concentrations 25 to 50 [micro]g/ml) but interfered with H5N1 replication and H5N1-induced apoptosis to a lesser extent (effective glycyrrhizin concentrations 100 [micro]g/ml or higher). Glycyrrhizin also diminished monocyte migration towards supernatants of H5N1-infected A549 cells. The mechanism by which glycyrrhizin interferes with H5N1 replication and H5N1-induced pro-inflammatory gene expression includes inhibition of H5N1-induced formation of reactive oxygen species and (in turn) reduced activation of NF[kappa]B, JNK, and p38, redox-sensitive signalling events known to be relevant for influenza A virus replication. Therefore, glycyrrhizin may complement the arsenal of potential drugs for the treatment of H5N1 disease.
    Keywords: Antiviral Agents -- Health Aspects ; Virus Replication -- Health Aspects ; Avian Influenza Viruses -- Health Aspects ; Avian Influenza -- Health Aspects ; Genes -- Health Aspects ; Apoptosis -- Health Aspects ; Gene Expression -- Health Aspects
    ISSN: 1932-6203
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  • 8
    Language: English
    In: Antiviral Research, 1999, Vol.44(1), pp.55-65
    Description: Cytomegalovirus (CMV) infection is a major problem in the immunosuppressed patient. It is thought that besides direct CMV induced cell lysis, immunological damage is part of CMV pathogenesis. New antiviral drugs, which combine immunomodulating and antiviral qualities, could be beneficial. Recently, it has been described that desferrioxamine (DFO) and calcium trinatrium diethylenetriaminepentaacetic acid (DTPA) exhibit both properties. In this report the antiviral effects of both compounds against rat CMV (RCMV) are described in vitro and in vivo using a generalised and local infection model. In vitro , both compounds exhibited a significant antiviral effect, DTPA being more potent than DFO. However, in the generalised infection model no effect was seen on mortality, morbidity or presence of virus in internal organs. In rats infected subcutaneously in the hind paw, no effect was seen locally on paw thickness, presence of viral antigens and inflammatory response. In addition, these rats suffered from a generalised infection of low magnitude at 15 days post infection, although both DFO and DTPA were able to lower the level of viral replication. In conclusion, our data indicate that despite in vitro activity, in vivo usage of DFO or DTPA for acute CMV infection is not warranted.
    Keywords: Rat Cytomegalovirus ; Dfo ; Dtpa ; In Vitro ; In Vivo ; Medicine ; Biology
    ISSN: 0166-3542
    E-ISSN: 1872-9096
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  • 9
    Language: English
    In: The American Journal of Pathology, 1999, Vol.155(1), pp.285-292
    Description: Thrombospondin-1 (TSP-1) is a potent inhibitor of angiogenesis. It has been shown that promoter sequences of the TSP-1 gene can be transactivated by the wild-type tumor suppressor protein p53. As human cytomegalovirus (HCMV) infection inactivates wild-type p53 of various cell types, we investigated whether HCMV infection is associated with reduced TSP-1 production. We found, in conjunction with accumulated p53, that TSP-1 mRNA and protein expression was significantly reduced in HCMV-infected cultured human fibroblasts. To determine whether the observed TSP-1 suppression depends on p53 inactivation, the p53-defective astrocytoma cell line U373MG was infected with HCMV. In these cells TSP-1 expression was also significantly reduced by HCMV infection whereas expression of the p53 mutant variant remained unaltered. In both cell lines the decreased expression of TSP-1 mRNA occurred early after infection (4 hours), indicating that HCMV inhibits TSP-1 transcription during the immediate-early phase of infection before HCMV DNA replication. Inhibition of HCMV DNA synthesis by ganciclovir did not influence TSP-1 reduction whereas the antisense oligonucleotide ISIS 2922, complementary to HCMV immediate-early mRNA, completely prevented the HCMV-mediated TSP-1 suppression. These findings strongly suggest a novel role for HCMV in the modulation of angiogenesis due to p53-independent down-regulation of TSP-1 expression.
    Keywords: Medicine
    ISSN: 0002-9440
    E-ISSN: 1525-2191
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  • 10
    Language: English
    In: Cellular and molecular life sciences CMLS, 2011, Vol.68(6), pp.1079-1090
    Description: Human cytomegalovirus (HCMV) is a major pathogen in immunocompromised individuals. Here, non-toxic concentrations of the anti-cancer kinase inhibitor sorafenib were shown to inhibit replication of different HCMV strains (including a ganciclovir-resistant strain) in different cell types. In contrast to established anti-HCMV drugs, sorafenib inhibited HCMV major immediate early promoter activity and HCMV immediate early antigen (IEA) expression. Sorafenib is known to inhibit Raf. Comparison of sorafenib with the MEK inhibitor U0126 suggested that sorafenib inhibits HCMV IEA expression through inhibition of Raf but independently of signaling through the Raf downstream kinase MEK 1/2. In concordance, siRNA-mediated depletion of Raf but not of MEK-reduced IEA expression. In conclusion, sorafenib diminished HCMV replication in clinically relevant concentrations and inhibited HCMV IEA expression, a pathophysiologically relevant event that is not affected by established anti-HCMV drugs. Moreover, we demonstrated for the first time that Raf activation is involved in HCMV IEA expression. ; Includes references ; p. 1079-1090.
    Keywords: Human Herpesvirus 5 ; Raf ; Antiviral Therapy ; Immediate Early Antigen ; Cancer Chemotherapy ; Kinase Inhibitor ; Sorafenib ; Oncomodulation
    ISSN: 1420-682X
    E-ISSN: 14209071
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