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Jiří Halouzka - One of the best experts on this subject based on the ideXlab platform.
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west nile fever a reemerging mosquito borne Viral Disease in europe
Emerging Infectious Diseases, 1999Co-Authors: Zdeněk Hubálek, Jiří HalouzkaAbstract:The 1996-97 outbreak of West Nile fever in and near Bucharest, Romania, with more than 500 clinical cases and a case-fatality rate approaching 10% (1-3), was the largest outbreak of arboViral illness in Europe since the OckelboPogosta-Karelian fever epidemic caused by Sindbis virus in northern Europe in the 1980s. This latest outbreak reaffirmed that mosquitoborne Viral Diseases may occur on a mass scale, even in temperate climates. West Nile virus is a member of the Japanese encephalitis antigenic complex of the genus Flavivirus, family Flaviviridae (4). All known members of this complex (Alfuy, Japanese encephalitis, Kokobera, Koutango, Kunjin, Murray Valley encephalitis, St. Louis encephalitis, Stratford, Usutu, and West Nile viruses) are transmissible by mosquitoes and many of them can cause febrile, sometimes fatal, illnesses in humans. West Nile virus was first isolated from the blood of a febrile woman in the West Nile district of Uganda in 1937 (5) and was subsequently isolated from patients, birds, and mosquitoes in Egypt in the early 1950s (6-7). The virus was soon recognized as the most widespread of the flaviviruses, with geographic distribution including Africa and Eurasia. Outside Europe (Figure), the virus has been reported from Algeria, Asian Russia, Azerbaijan, Botswana, Central African Republic, Cote dIvoire, Cyprus, Democratic Republic of Congo (former Zaire), Egypt, Ethiopia, India, Israel, Kazakhstan, Madagascar, Morocco, Mozambique, Nigeria, Pakistan, Senegal, South Africa, Tajikistan, Turkmenia, Uganda, and Uzbekistan. Furthermore, West Nile virus antibodies have been detected in human sera from Armenia, Borneo, China, Georgia, Iraq, Kenya, Lebanon, Malaysia, the Philippines, Sri Lanka, Sudan, Syria, Thailand, Tunisia, and Turkey (8-10). Kunjin virus is closely related to West Nile virus (11,12), representing a counterpart or subtype for Australia and Southeast Asia; some West Nile West Nile Fever—a Reemerging Mosquito-Borne Viral Disease in Europe
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West Nile fever--a reemerging mosquito-borne Viral Disease in Europe.
Emerging infectious diseases, 1999Co-Authors: Zdeněk Hubálek, Jiří HalouzkaAbstract:West Nile virus causes sporadic cases and outbreaks of human and equine Disease in Europe (western Mediterranean and southern Russia in 1962-64, Belarus and Ukraine in the 1970s and 1980s, Romania in 1996-97, Czechland in 1997, and Italy in 1998). Environmental factors, including human activities, that enhance population densities of vector mosquitoes (heavy rains followed by floods, irrigation, higher than usual temperature, or formation of ecologic niches that enable mass breeding of mosquitoes) could increase the incidence of West Nile fever.
Zdeněk Hubálek - One of the best experts on this subject based on the ideXlab platform.
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west nile fever a reemerging mosquito borne Viral Disease in europe
Emerging Infectious Diseases, 1999Co-Authors: Zdeněk Hubálek, Jiří HalouzkaAbstract:The 1996-97 outbreak of West Nile fever in and near Bucharest, Romania, with more than 500 clinical cases and a case-fatality rate approaching 10% (1-3), was the largest outbreak of arboViral illness in Europe since the OckelboPogosta-Karelian fever epidemic caused by Sindbis virus in northern Europe in the 1980s. This latest outbreak reaffirmed that mosquitoborne Viral Diseases may occur on a mass scale, even in temperate climates. West Nile virus is a member of the Japanese encephalitis antigenic complex of the genus Flavivirus, family Flaviviridae (4). All known members of this complex (Alfuy, Japanese encephalitis, Kokobera, Koutango, Kunjin, Murray Valley encephalitis, St. Louis encephalitis, Stratford, Usutu, and West Nile viruses) are transmissible by mosquitoes and many of them can cause febrile, sometimes fatal, illnesses in humans. West Nile virus was first isolated from the blood of a febrile woman in the West Nile district of Uganda in 1937 (5) and was subsequently isolated from patients, birds, and mosquitoes in Egypt in the early 1950s (6-7). The virus was soon recognized as the most widespread of the flaviviruses, with geographic distribution including Africa and Eurasia. Outside Europe (Figure), the virus has been reported from Algeria, Asian Russia, Azerbaijan, Botswana, Central African Republic, Cote dIvoire, Cyprus, Democratic Republic of Congo (former Zaire), Egypt, Ethiopia, India, Israel, Kazakhstan, Madagascar, Morocco, Mozambique, Nigeria, Pakistan, Senegal, South Africa, Tajikistan, Turkmenia, Uganda, and Uzbekistan. Furthermore, West Nile virus antibodies have been detected in human sera from Armenia, Borneo, China, Georgia, Iraq, Kenya, Lebanon, Malaysia, the Philippines, Sri Lanka, Sudan, Syria, Thailand, Tunisia, and Turkey (8-10). Kunjin virus is closely related to West Nile virus (11,12), representing a counterpart or subtype for Australia and Southeast Asia; some West Nile West Nile Fever—a Reemerging Mosquito-Borne Viral Disease in Europe
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West Nile fever--a reemerging mosquito-borne Viral Disease in Europe.
Emerging infectious diseases, 1999Co-Authors: Zdeněk Hubálek, Jiří HalouzkaAbstract:West Nile virus causes sporadic cases and outbreaks of human and equine Disease in Europe (western Mediterranean and southern Russia in 1962-64, Belarus and Ukraine in the 1970s and 1980s, Romania in 1996-97, Czechland in 1997, and Italy in 1998). Environmental factors, including human activities, that enhance population densities of vector mosquitoes (heavy rains followed by floods, irrigation, higher than usual temperature, or formation of ecologic niches that enable mass breeding of mosquitoes) could increase the incidence of West Nile fever.
Stephanie Dupuis - One of the best experts on this subject based on the ideXlab platform.
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impaired response to interferon alpha beta and lethal Viral Disease in human stat1 deficiency
Nature Genetics, 2003Co-Authors: Stephanie Dupuis, Emmanuelle Jouanguy, Sami Alhajjar, Claire Fieschi, Ibrahim Almohsen, Suliman Aljumaah, Kun Yang, Ariane Chapgier, Celine Eidenschenk, Abdulaziz Al GhonaiumAbstract:The receptors for interferon-α/β (IFN-α/β) and IFN-γ activate components of the Janus kinase–signal transducer and activator of transcription (JAK–STAT) signaling pathway, leading to the formation of at least two transcription factor complexes1. STAT1 interacts with STAT2 and p48/IRF-9 to form the transcription factor IFN-stimulated gene factor 3 (ISGF3). STAT1 dimers form γ-activated factor (GAF). ISGF3 is induced mainly by IFN-α/β, and GAF by IFN-γ, although both factors can be activated by both types of IFN. Individuals with mutations in either chain of the IFN-γ receptor (IFN-γR) are susceptible to infection with mycobacteria2,3,4,5. A heterozygous STAT1 mutation that impairs GAF but not ISGF3 activation has been found in other individuals with mycobacterial Disease6. No individuals with deleterious mutations in the IFN-α/β signaling pathway have been described. We report here two unrelated infants homozygous with respect to mutated STAT1 alleles. Neither IFN-α/β nor IFN-γ activated STAT1-containing transcription factors. Like individuals with IFN-γR deficiency, both infants suffered from mycobacterial Disease, but unlike individuals with IFN-γR deficiency, both died of Viral Disease. Viral multiplication was not inhibited by recombinant IFN-α/β in cell lines from the two individuals. Inherited impairment of the STAT1-dependent response to human IFN-α/β thus results in susceptibility to Viral Disease.
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impaired response to interferon alpha beta and lethal Viral Disease in human stat1 deficiency
Nature Genetics, 2003Co-Authors: Stephanie Dupuis, Emmanuelle Jouanguy, Sami Alhajjar, Claire Fieschi, Ibrahim Almohsen, Suliman Aljumaah, Kun Yang, Ariane Chapgier, Celine Eidenschenk, Pierre EidAbstract:The receptors for interferon-alpha/beta (IFN-alpha/beta) and IFN-gamma activate components of the Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway, leading to the formation of at least two transcription factor complexes. STAT1 interacts with STAT2 and p48/IRF-9 to form the transcription factor IFN-stimulated gene factor 3 (ISGF3). STAT1 dimers form gamma-activated factor (GAF). ISGF3 is induced mainly by IFN-alpha/beta, and GAF by IFN-gamma, although both factors can be activated by both types of IFN. Individuals with mutations in either chain of the IFN-gamma receptor (IFN-gammaR) are susceptible to infection with mycobacteria. A heterozygous STAT1 mutation that impairs GAF but not ISGF3 activation has been found in other individuals with mycobacterial Disease. No individuals with deleterious mutations in the IFN-alpha/beta signaling pathway have been described. We report here two unrelated infants homozygous with respect to mutated STAT1 alleles. Neither IFN-alpha/beta nor IFN-gamma activated STAT1-containing transcription factors. Like individuals with IFN-gammaR deficiency, both infants suffered from mycobacterial Disease, but unlike individuals with IFN-gammaR deficiency, both died of Viral Disease. Viral multiplication was not inhibited by recombinant IFN-alpha/beta in cell lines from the two individuals. Inherited impairment of the STAT1-dependent response to human IFN-alpha/beta thus results in susceptibility to Viral Disease.
David E Levy - One of the best experts on this subject based on the ideXlab platform.
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targeted disruption of the mouse stat1 gene results in compromised innate immunity to Viral Disease
Cell, 1996Co-Authors: Joan E Durbin, Renee Hackenmiller, Celeste M Simon, David E LevyAbstract:The STAT1 transcription factor is activated in response to many cytokines and growth factors. To study the requirement for STAT1 in vivo, we disrupted the Stat1 gene in embryonic stem (ES) cells and in mice. Stat1(-1-)ES cells were unresponsive to interferon (IFN), but retained responsiveness to leukemia inhibitory factor (LIF) and remained LIF dependent for undifferentiated growth. Stat1(-1-1) animals were born at normal frequencies and displayed no gross developmental defects. However, these animals failed to thrive and were extremely susceptible to Viral Disease. Cells and tissues from Stat1(-1-) mice were unresponsive to IFN, but remained responsive to all other cytokines tested. Thus, STAT1 appears to be specific for IFN pathways that are essential for viability in the face of otherwise innocuous pathogens.
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targeted disruption of the mouse stat1 gene results in compromised innate immunity to Viral Disease
Cell, 1996Co-Authors: Joan E Durbin, Renee Hackenmiller, Celeste M Simon, David E LevyAbstract:Abstract The STAT1 transcription factor is activated in response to many cytokines and growth factors. To study the requirement for STAT1 in vivo, we disrupted the Stat1 gene in embryonic stem (ES) cells and in mice. Stat1 −/− ES cells were unresponsive to interferon (IFN), but retained responsiveness to leukemia inhibitory factor (LIF) and remained LIF dependent for undifferentiated growth. Stat1 −/− animals were born at normal frequencies and displayed no gross developmental defects. However, these animals failed to thrive and were extremely susceptible to Viral Disease. Cells and tissues from Stat1 −/− mice were unresponsive to IFN, but remained responsive to all other cytokines tested. Thus, STAT1 appears to be specific for IFN pathways that are essential for viability in the face of otherwise innocuous pathogens.
Pierre Eid - One of the best experts on this subject based on the ideXlab platform.
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impaired response to interferon alpha beta and lethal Viral Disease in human stat1 deficiency
Nature Genetics, 2003Co-Authors: Stephanie Dupuis, Emmanuelle Jouanguy, Sami Alhajjar, Claire Fieschi, Ibrahim Almohsen, Suliman Aljumaah, Kun Yang, Ariane Chapgier, Celine Eidenschenk, Pierre EidAbstract:The receptors for interferon-alpha/beta (IFN-alpha/beta) and IFN-gamma activate components of the Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway, leading to the formation of at least two transcription factor complexes. STAT1 interacts with STAT2 and p48/IRF-9 to form the transcription factor IFN-stimulated gene factor 3 (ISGF3). STAT1 dimers form gamma-activated factor (GAF). ISGF3 is induced mainly by IFN-alpha/beta, and GAF by IFN-gamma, although both factors can be activated by both types of IFN. Individuals with mutations in either chain of the IFN-gamma receptor (IFN-gammaR) are susceptible to infection with mycobacteria. A heterozygous STAT1 mutation that impairs GAF but not ISGF3 activation has been found in other individuals with mycobacterial Disease. No individuals with deleterious mutations in the IFN-alpha/beta signaling pathway have been described. We report here two unrelated infants homozygous with respect to mutated STAT1 alleles. Neither IFN-alpha/beta nor IFN-gamma activated STAT1-containing transcription factors. Like individuals with IFN-gammaR deficiency, both infants suffered from mycobacterial Disease, but unlike individuals with IFN-gammaR deficiency, both died of Viral Disease. Viral multiplication was not inhibited by recombinant IFN-alpha/beta in cell lines from the two individuals. Inherited impairment of the STAT1-dependent response to human IFN-alpha/beta thus results in susceptibility to Viral Disease.
