The Experts below are selected from a list of 324 Experts worldwide ranked by ideXlab platform
Houssam Attoui - One of the best experts on this subject based on the ideXlab platform.
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Immunisation with bacterial expressed VP2 and VP5 of bluetongue virus (BTV) protect α/β Interferon-Receptor knock-out (IFNAR(-/-)) mice from homologous lethal challenge.
Vaccine, 2014Co-Authors: Fauziah Mohd Jaafar, Peter P. C. Mertens, Mourad Belhouchet, Damien Vitour, Micheline Adam, Emmanuel Bréard, Stéphan Zientara, Houssam AttouiAbstract:BTV-4 structural proteins VP2 (as two domains: VP2D1 and VP2D2), VP5 (lacking the first 100 amino acids: VP5Δ1-100) and full-length VP7, expressed in bacteria as soluble glutathione S-transferase (GST) fusion-proteins, were used to immunise Balb/c and α/β Interferon Receptor knock-out (IFNAR(-/-)) mice. Neutralising antibody (NAbs) titres (expressed as log10 of the reciprocal of the last dilution of mouse serum which reduced plaque number by ≥50%) induced by the VP2 domains ranged from 1.806 to 2.408 in Balb/c and IFNAR(-/-) mice. The immunised IFNAR(-/-) mice challenged with a homologous live BTV-4 survived and failed to develop signs of infection (ocular discharge and apathy). Although subsequent attempts to isolate virus were unsuccessful (possibly reflecting presence of neutralising antibodies), a transient/low level viraemia was detected by real time RT-PCR. In contrast, mice immunised with the two VP2 domains with or without VP5Δ1-100 and VP7, then challenged with the heterologous serotype, BTV-8, all died by day 7 post-infection. We conclude that immunisation with bacterially-expressed VP2 domains can induce strong serotype-specific NAb responses. Bacterial expression could represent a cost effective and risk-free alternative to the use of live or inactivated vaccines, particularly if viruses prove to be difficult to propagate in cell culture (like BTV-25). A vaccine based on bacterially expressed VP2 and VP5 of BTV is also DIVA-compatible.
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Immunisation with bacterial expressed VP2 and VP5 of bluetongue virus (BTV) protect α/β Interferon-Receptor knock-out (IFNAR−/−) mice from homologous lethal challenge
Vaccine, 2014Co-Authors: Fauziah Mohd Jaafar, Peter P. C. Mertens, Mourad Belhouchet, Damien Vitour, Micheline Adam, Emmanuel Bréard, Stéphan Zientara, Houssam AttouiAbstract:BTV-4 structural proteins VP2 (as two domains: VP2D1 and VP2D2), VP5 (lacking the first 100 amino acids: VP5(Delta 1-100)) and full-length VP7, expressed in bacteria as soluble glutathione S-transferase (GST) fusion-proteins, were used to immunise Balb/c and alpha/beta Interferon Receptor knock-out (IFNAR(-/-)) mice. Neutralising antibody (NAbs) titres (expressed as log(10) of the reciprocal of the last dilution of mouse serum which reduced plaque number by >= 50%) induced by the VP2 domains ranged from 1.806 to 2.408 in Balb/c and IFNAR(-/-) mice. The immunised IFNAR(-/-) mice challenged with a homologous live BTV-4 survived and failed to develop signs of infection (ocular discharge and apathy). Although subsequent attempts to isolate virus were unsuccessful (possibly reflecting presence of neutralising antibodies), a transient/low level viraemia was detected by real time RT-PCR. In contrast, mice immunised with the two VP2 domains with or without VP5(Delta 1-100) and VP7, then challenged with the heterologous serotype, BTV-8, all died by day 7 post-infection. We conclude that immunisation with bacterially-expressed VP2 domains can induce strong serotype-specific NAb responses. Bacterial expression could represent a cost effective and risk-free alternative to the use of live or inactivated vaccines, particularly if viruses prove to be difficult to propagate in cell culture (like BTV-25). A vaccine based on bacterially expressed VP2 and VP5 of BTV is also DIVA-compatible.
Shigeru Marubashi - One of the best experts on this subject based on the ideXlab platform.
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treatment of hepatocellular carcinoma with major portal vein thrombosis by combined therapy with subcutaneous Interferon alpha and intra arterial 5 fluorouracil role of type 1 Interferon Receptor expression
British Journal of Cancer, 2005Co-Authors: Hirofumi Ota, H. Nagano, Masato Sakon, Hidetoshi Eguchi, Motoi Kondo, Tameyoshi Yamamoto, Misuzu Nakamura, Bazarragchaa Damdinsuren, Hisashi Wada, Shigeru MarubashiAbstract:We previously reported the beneficial effects of combination therapy of Interferon (IFN)-α/5-fluorouracil (FU) for advanced hepatocellular carcinoma (HCC) with tumour thrombi in the major portal branches. This report describes the results of longer follow-up and includes more than double the number of patients relative to the original report, and evaluates the role of IFN-α/type 2 Interferon Receptor (IFNAR2) expression on the response to the combination therapy. The study subjects were 55 patients with advanced HCC and tumour thrombi in the major branches of the portal vein (Vp3 or 4). They were treated with at least two courses of IFN-α/5-FU without major complication. In the 55 patients, 24 (43.6%) showed objective response (eight (14.5%) showed complete response, 16 (29.1%) partial response), four (7.3%) showed no response, and 27 (49.1%) showed progressive disease. Immunohistochemically, IFNAR2 expression was detected in nine out of 13 (69.2%) patients. There was significant difference in the time-to-progression survival (P=0.0002) and the overall survival (P<0.0001) between IFNAR2-positive and -negative cases. There was a significant correlation between IFNAR2 expression and response to IFN-α/5-FU combination therapy in univariate analysis (P=0.0070). IFN-α/5-FU combination therapy is a promising modality for advanced HCC with tumour thrombi in the major portal branches and could significantly depend on IFNAR2 expression.
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Treatment of hepatocellular carcinoma with major portal vein thrombosis by combined therapy with subcutaneous Interferon-|[alpha]| and intra-arterial 5-fluorouracil; role of type 1 Interferon Receptor expression
British journal of cancer, 2005Co-Authors: Hirofumi Ota, H. Nagano, Masato Sakon, Hidetoshi Eguchi, Motoi Kondo, Tameyoshi Yamamoto, Misuzu Nakamura, Bazarragchaa Damdinsuren, Hisashi Wada, Shigeru MarubashiAbstract:We previously reported the beneficial effects of combination therapy of Interferon (IFN)-α/5-fluorouracil (FU) for advanced hepatocellular carcinoma (HCC) with tumour thrombi in the major portal branches. This report describes the results of longer follow-up and includes more than double the number of patients relative to the original report, and evaluates the role of IFN-α/type 2 Interferon Receptor (IFNAR2) expression on the response to the combination therapy. The study subjects were 55 patients with advanced HCC and tumour thrombi in the major branches of the portal vein (Vp3 or 4). They were treated with at least two courses of IFN-α/5-FU without major complication. In the 55 patients, 24 (43.6%) showed objective response (eight (14.5%) showed complete response, 16 (29.1%) partial response), four (7.3%) showed no response, and 27 (49.1%) showed progressive disease. Immunohistochemically, IFNAR2 expression was detected in nine out of 13 (69.2%) patients. There was significant difference in the time-to-progression survival (P=0.0002) and the overall survival (P
Juancarlos Saiz - One of the best experts on this subject based on the ideXlab platform.
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a recombinant dna vaccine protects mice deficient in the alpha beta Interferon Receptor against lethal challenge with usutu virus
Vaccine, 2016Co-Authors: Miguel A Martinacebes, Anabelen Blazquez, Rodrigo Canasarranz, Angela Vazquezcalvo, Teresa Merinoramos, Estela Escribanoromero, Francisco Sobrino, Juancarlos SaizAbstract:Abstract Usutu virus (USUV) is a mosquito-borne flavivirus whose circulation had been confined to Africa since it was first detected in 1959. However, in the last decade USUV has emerged in Europe causing episodes of avian mortality and sporadic severe neuroinvasive infections in humans. Remarkably, adult laboratory mice exhibit limited susceptibility to USUV infection, which has impaired the analysis of the immune responses, thus complicating the evaluation of virus–host interactions and of vaccine candidates against this pathogen. In this work, we showed that mice deficient in the alpha/beta Interferon Receptor (IFNAR (−/−) mice) were highly susceptible to USUV infection and provided a lethal challenge model for vaccine testing. To validate this infection model, a plasmid DNA vaccine candidate encoding the precursor of membrane (prM) and envelope (E) proteins of USUV was engineered. Transfection of cultured cells with this plasmid resulted in expression of USUV antigens and the assembly and secretion of small virus-like particles also known as recombinant subviral particles (RSPs). A single intramuscular immunization with this plasmid was sufficient to elicit a significant level of protection against challenge with USUV in IFNAR (−/−) mice. The characterization of the humoral response induced revealed that DNA vaccination primed anti-USUV antibodies, including neutralizing antibodies. Overall, these results probe the suitability of IFNAR (−/−) mice as an amenable small animal model for the study of USUV host virus interactions and vaccine testing, as well as the feasibility of DNA-based vaccine strategies for the control of this pathogen.
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A recombinant DNA vaccine protects mice deficient in the alpha/beta Interferon Receptor against lethal challenge with Usutu virus.
Vaccine, 2016Co-Authors: Miguel A. Martín-acebes, Anabelen Blazquez, Francisco Sobrino, Rodrigo Cañas-arranz, Ángela Vázquez-calvo, Teresa Merino-ramos, Estela Escribano-romero, Juancarlos SaizAbstract:Usutu virus (USUV) is a mosquito-borne flavivirus whose circulation had been confined to Africa since it was first detected in 1959. However, in the last decade USUV has emerged in Europe causing episodes of avian mortality and sporadic severe neuroinvasive infections in humans. Remarkably, adult laboratory mice exhibit limited susceptibility to USUV infection, which has impaired the analysis of the immune responses, thus complicating the evaluation of virus-host interactions and of vaccine candidates against this pathogen. In this work, we showed that mice deficient in the alpha/beta Interferon Receptor (IFNAR (-/-) mice) were highly susceptible to USUV infection and provided a lethal challenge model for vaccine testing. To validate this infection model, a plasmid DNA vaccine candidate encoding the precursor of membrane (prM) and envelope (E) proteins of USUV was engineered. Transfection of cultured cells with this plasmid resulted in expression of USUV antigens and the assembly and secretion of small virus-like particles also known as recombinant subviral particles (RSPs). A single intramuscular immunization with this plasmid was sufficient to elicit a significant level of protection against challenge with USUV in IFNAR (-/-) mice. The characterization of the humoral response induced revealed that DNA vaccination primed anti-USUV antibodies, including neutralizing antibodies. Overall, these results probe the suitability of IFNAR (-/-) mice as an amenable small animal model for the study of USUV host virus interactions and vaccine testing, as well as the feasibility of DNA-based vaccine strategies for the control of this pathogen.
Peter P. C. Mertens - One of the best experts on this subject based on the ideXlab platform.
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Immunisation with bacterial expressed VP2 and VP5 of bluetongue virus (BTV) protect α/β Interferon-Receptor knock-out (IFNAR(-/-)) mice from homologous lethal challenge.
Vaccine, 2014Co-Authors: Fauziah Mohd Jaafar, Peter P. C. Mertens, Mourad Belhouchet, Damien Vitour, Micheline Adam, Emmanuel Bréard, Stéphan Zientara, Houssam AttouiAbstract:BTV-4 structural proteins VP2 (as two domains: VP2D1 and VP2D2), VP5 (lacking the first 100 amino acids: VP5Δ1-100) and full-length VP7, expressed in bacteria as soluble glutathione S-transferase (GST) fusion-proteins, were used to immunise Balb/c and α/β Interferon Receptor knock-out (IFNAR(-/-)) mice. Neutralising antibody (NAbs) titres (expressed as log10 of the reciprocal of the last dilution of mouse serum which reduced plaque number by ≥50%) induced by the VP2 domains ranged from 1.806 to 2.408 in Balb/c and IFNAR(-/-) mice. The immunised IFNAR(-/-) mice challenged with a homologous live BTV-4 survived and failed to develop signs of infection (ocular discharge and apathy). Although subsequent attempts to isolate virus were unsuccessful (possibly reflecting presence of neutralising antibodies), a transient/low level viraemia was detected by real time RT-PCR. In contrast, mice immunised with the two VP2 domains with or without VP5Δ1-100 and VP7, then challenged with the heterologous serotype, BTV-8, all died by day 7 post-infection. We conclude that immunisation with bacterially-expressed VP2 domains can induce strong serotype-specific NAb responses. Bacterial expression could represent a cost effective and risk-free alternative to the use of live or inactivated vaccines, particularly if viruses prove to be difficult to propagate in cell culture (like BTV-25). A vaccine based on bacterially expressed VP2 and VP5 of BTV is also DIVA-compatible.
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Immunisation with bacterial expressed VP2 and VP5 of bluetongue virus (BTV) protect α/β Interferon-Receptor knock-out (IFNAR−/−) mice from homologous lethal challenge
Vaccine, 2014Co-Authors: Fauziah Mohd Jaafar, Peter P. C. Mertens, Mourad Belhouchet, Damien Vitour, Micheline Adam, Emmanuel Bréard, Stéphan Zientara, Houssam AttouiAbstract:BTV-4 structural proteins VP2 (as two domains: VP2D1 and VP2D2), VP5 (lacking the first 100 amino acids: VP5(Delta 1-100)) and full-length VP7, expressed in bacteria as soluble glutathione S-transferase (GST) fusion-proteins, were used to immunise Balb/c and alpha/beta Interferon Receptor knock-out (IFNAR(-/-)) mice. Neutralising antibody (NAbs) titres (expressed as log(10) of the reciprocal of the last dilution of mouse serum which reduced plaque number by >= 50%) induced by the VP2 domains ranged from 1.806 to 2.408 in Balb/c and IFNAR(-/-) mice. The immunised IFNAR(-/-) mice challenged with a homologous live BTV-4 survived and failed to develop signs of infection (ocular discharge and apathy). Although subsequent attempts to isolate virus were unsuccessful (possibly reflecting presence of neutralising antibodies), a transient/low level viraemia was detected by real time RT-PCR. In contrast, mice immunised with the two VP2 domains with or without VP5(Delta 1-100) and VP7, then challenged with the heterologous serotype, BTV-8, all died by day 7 post-infection. We conclude that immunisation with bacterially-expressed VP2 domains can induce strong serotype-specific NAb responses. Bacterial expression could represent a cost effective and risk-free alternative to the use of live or inactivated vaccines, particularly if viruses prove to be difficult to propagate in cell culture (like BTV-25). A vaccine based on bacterially expressed VP2 and VP5 of BTV is also DIVA-compatible.
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Immunization of knock-out α/β Interferon Receptor mice against lethal bluetongue infection with a BoHV-4-based vector expressing BTV-8 VP2 antigen.
Vaccine, 2011Co-Authors: Valentina Franceschi, Antonio Capocefalo, Eva Calvo-pinilla, Marco Redaelli, Carla Mucignat-caretta, Peter P. C. Mertens, Javier Ortego, Gaetano DonofrioAbstract:Abstract New effective tools for vaccine strategies are necessary to limit the spread of bluetongue, an insect-transmitted viral disease of domestic and wild ruminants. In the present study, BoHV-4-based vector cloned as a bacterial artificial chromosome (BAC) was engineered to express the bluetongue virus (BTV) immune-dominant glycoprotein VP2 provided of a heterologous signal peptide to its amino terminal and a trans-membrane domain to its carboxyl terminal (IgK-VP2gDtm), to allow the VP2 expression targeting to the cell membrane fraction. Based on adult α/β Interferon Receptor knockout (IFNAR (−/−) ) mice, a newly generated bluetongue laboratory animal model, a pre-challenge experiment was performed to test BoHV-4 safety on such immune-compromised animal. BoHV-4 infected IFNAR (−/−) mice did not show clinical signs even following the inoculation of BoHV-4 intra-cerebrally, although many areas of the brain got transduced. IFNAR (−/−) mice intraperitoneally inoculated twice with BoHV-4-A-IgK-VP2gDtm at different time points developed serum neutralizing antibodies against BTV and showed a strongly reduced viremia and a longer survival time when challenged with a lethal dose of BTV-8. The data acquired in this pilot study validate BoHV-4-based vector as a safe and effective heterologous antigen carrier/producer for the formulation of enhanced recombinant immunogens for the vaccination against lethal bluetongue.
Fauziah Mohd Jaafar - One of the best experts on this subject based on the ideXlab platform.
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Immunisation with bacterial expressed VP2 and VP5 of bluetongue virus (BTV) protect α/β Interferon-Receptor knock-out (IFNAR(-/-)) mice from homologous lethal challenge.
Vaccine, 2014Co-Authors: Fauziah Mohd Jaafar, Peter P. C. Mertens, Mourad Belhouchet, Damien Vitour, Micheline Adam, Emmanuel Bréard, Stéphan Zientara, Houssam AttouiAbstract:BTV-4 structural proteins VP2 (as two domains: VP2D1 and VP2D2), VP5 (lacking the first 100 amino acids: VP5Δ1-100) and full-length VP7, expressed in bacteria as soluble glutathione S-transferase (GST) fusion-proteins, were used to immunise Balb/c and α/β Interferon Receptor knock-out (IFNAR(-/-)) mice. Neutralising antibody (NAbs) titres (expressed as log10 of the reciprocal of the last dilution of mouse serum which reduced plaque number by ≥50%) induced by the VP2 domains ranged from 1.806 to 2.408 in Balb/c and IFNAR(-/-) mice. The immunised IFNAR(-/-) mice challenged with a homologous live BTV-4 survived and failed to develop signs of infection (ocular discharge and apathy). Although subsequent attempts to isolate virus were unsuccessful (possibly reflecting presence of neutralising antibodies), a transient/low level viraemia was detected by real time RT-PCR. In contrast, mice immunised with the two VP2 domains with or without VP5Δ1-100 and VP7, then challenged with the heterologous serotype, BTV-8, all died by day 7 post-infection. We conclude that immunisation with bacterially-expressed VP2 domains can induce strong serotype-specific NAb responses. Bacterial expression could represent a cost effective and risk-free alternative to the use of live or inactivated vaccines, particularly if viruses prove to be difficult to propagate in cell culture (like BTV-25). A vaccine based on bacterially expressed VP2 and VP5 of BTV is also DIVA-compatible.
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Immunisation with bacterial expressed VP2 and VP5 of bluetongue virus (BTV) protect α/β Interferon-Receptor knock-out (IFNAR−/−) mice from homologous lethal challenge
Vaccine, 2014Co-Authors: Fauziah Mohd Jaafar, Peter P. C. Mertens, Mourad Belhouchet, Damien Vitour, Micheline Adam, Emmanuel Bréard, Stéphan Zientara, Houssam AttouiAbstract:BTV-4 structural proteins VP2 (as two domains: VP2D1 and VP2D2), VP5 (lacking the first 100 amino acids: VP5(Delta 1-100)) and full-length VP7, expressed in bacteria as soluble glutathione S-transferase (GST) fusion-proteins, were used to immunise Balb/c and alpha/beta Interferon Receptor knock-out (IFNAR(-/-)) mice. Neutralising antibody (NAbs) titres (expressed as log(10) of the reciprocal of the last dilution of mouse serum which reduced plaque number by >= 50%) induced by the VP2 domains ranged from 1.806 to 2.408 in Balb/c and IFNAR(-/-) mice. The immunised IFNAR(-/-) mice challenged with a homologous live BTV-4 survived and failed to develop signs of infection (ocular discharge and apathy). Although subsequent attempts to isolate virus were unsuccessful (possibly reflecting presence of neutralising antibodies), a transient/low level viraemia was detected by real time RT-PCR. In contrast, mice immunised with the two VP2 domains with or without VP5(Delta 1-100) and VP7, then challenged with the heterologous serotype, BTV-8, all died by day 7 post-infection. We conclude that immunisation with bacterially-expressed VP2 domains can induce strong serotype-specific NAb responses. Bacterial expression could represent a cost effective and risk-free alternative to the use of live or inactivated vaccines, particularly if viruses prove to be difficult to propagate in cell culture (like BTV-25). A vaccine based on bacterially expressed VP2 and VP5 of BTV is also DIVA-compatible.