The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
Brian H Bird - One of the best experts on this subject based on the ideXlab platform.
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rift valley fever virus lacking nsm proteins retains high virulence in vivo and may provide a model of human delayed onset Neurologic Disease
Virology, 2007Co-Authors: Brian H Bird, Cesar G Albarino, Stuart T NicholAbstract:Rift Valley fever virus is a significant human and veterinary pathogen responsible for explosive outbreaks throughout Africa and the Arabian Peninsula. Severe acute Disease in humans includes rapid onset hepatic Disease and hemorrhagic fever or delayed onset encephalitis. A highly efficient reverse genetics system was developed which allowed generation of recombinant RVF viruses to assess the role of NSm protein in virulence in a rat model in which wild-type RVF virus strain ZH501 (wt-ZH501) results in 100% lethal hepatic Disease 2-3 days post infection. While extensive genomic analysis indicates conservation of the NSm coding capability of diverse RVF viruses, and viruses deficient in NSs proteins are completely attenuated in vivo, comparison of wt-ZH501, a reverse genetics generated wt-ZH501 virus (R-ZH501), and R-ZH501 virus lacking the NSm proteins (R-DeltaNSm-ZH501) demonstrated that the NSm proteins were nonessential for in vivo virulence and lethality. Surprisingly, while 44% of R-DeltaNSm-ZH501 infected animals quickly developed lethal hepatic Disease similar to wt- and R-ZH501, 17% developed delayed onset Neurologic Disease (lethargy, head tremors, and ataxia) at 13 days post infection. Such infections may provide the basis for study of both RVF acute hepatic Disease and delayed onset encephalitic Disease in humans.
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rift valley fever virus lacking nsm proteins retains high virulence in vivo and may provide a model of human delayed onset Neurologic Disease
Virology, 2007Co-Authors: Brian H Bird, Cesar G Albarino, Stuart T NicholAbstract:Abstract Rift Valley fever virus is a significant human and veterinary pathogen responsible for explosive outbreaks throughout Africa and the Arabian Peninsula. Severe acute Disease in humans includes rapid onset hepatic Disease and hemorrhagic fever or delayed onset encephalitis. A highly efficient reverse genetics system was developed which allowed generation of recombinant RVF viruses to assess the role of NSm protein in virulence in a rat model in which wild-type RVF virus strain ZH501 (wt-ZH501) results in 100% lethal hepatic Disease 2–3 days post infection. While extensive genomic analysis indicates conservation of the NSm coding capability of diverse RVF viruses, and viruses deficient in NSs proteins are completely attenuated in vivo , comparison of wt-ZH501, a reverse genetics generated wt-ZH501 virus (R-ZH501), and R-ZH501 virus lacking the NSm proteins (R-ΔNSm-ZH501) demonstrated that the NSm proteins were nonessential for in vivo virulence and lethality. Surprisingly, while 44% of R-ΔNSm-ZH501 infected animals quickly developed lethal hepatic Disease similar to wt- and R-ZH501, 17% developed delayed onset Neurologic Disease (lethargy, head tremors, and ataxia) at 13 days post infection. Such infections may provide the basis for study of both RVF acute hepatic Disease and delayed onset encephalitic Disease in humans.
Stuart T Nichol - One of the best experts on this subject based on the ideXlab platform.
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rift valley fever virus lacking nsm proteins retains high virulence in vivo and may provide a model of human delayed onset Neurologic Disease
Virology, 2007Co-Authors: Brian H Bird, Cesar G Albarino, Stuart T NicholAbstract:Rift Valley fever virus is a significant human and veterinary pathogen responsible for explosive outbreaks throughout Africa and the Arabian Peninsula. Severe acute Disease in humans includes rapid onset hepatic Disease and hemorrhagic fever or delayed onset encephalitis. A highly efficient reverse genetics system was developed which allowed generation of recombinant RVF viruses to assess the role of NSm protein in virulence in a rat model in which wild-type RVF virus strain ZH501 (wt-ZH501) results in 100% lethal hepatic Disease 2-3 days post infection. While extensive genomic analysis indicates conservation of the NSm coding capability of diverse RVF viruses, and viruses deficient in NSs proteins are completely attenuated in vivo, comparison of wt-ZH501, a reverse genetics generated wt-ZH501 virus (R-ZH501), and R-ZH501 virus lacking the NSm proteins (R-DeltaNSm-ZH501) demonstrated that the NSm proteins were nonessential for in vivo virulence and lethality. Surprisingly, while 44% of R-DeltaNSm-ZH501 infected animals quickly developed lethal hepatic Disease similar to wt- and R-ZH501, 17% developed delayed onset Neurologic Disease (lethargy, head tremors, and ataxia) at 13 days post infection. Such infections may provide the basis for study of both RVF acute hepatic Disease and delayed onset encephalitic Disease in humans.
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rift valley fever virus lacking nsm proteins retains high virulence in vivo and may provide a model of human delayed onset Neurologic Disease
Virology, 2007Co-Authors: Brian H Bird, Cesar G Albarino, Stuart T NicholAbstract:Abstract Rift Valley fever virus is a significant human and veterinary pathogen responsible for explosive outbreaks throughout Africa and the Arabian Peninsula. Severe acute Disease in humans includes rapid onset hepatic Disease and hemorrhagic fever or delayed onset encephalitis. A highly efficient reverse genetics system was developed which allowed generation of recombinant RVF viruses to assess the role of NSm protein in virulence in a rat model in which wild-type RVF virus strain ZH501 (wt-ZH501) results in 100% lethal hepatic Disease 2–3 days post infection. While extensive genomic analysis indicates conservation of the NSm coding capability of diverse RVF viruses, and viruses deficient in NSs proteins are completely attenuated in vivo , comparison of wt-ZH501, a reverse genetics generated wt-ZH501 virus (R-ZH501), and R-ZH501 virus lacking the NSm proteins (R-ΔNSm-ZH501) demonstrated that the NSm proteins were nonessential for in vivo virulence and lethality. Surprisingly, while 44% of R-ΔNSm-ZH501 infected animals quickly developed lethal hepatic Disease similar to wt- and R-ZH501, 17% developed delayed onset Neurologic Disease (lethargy, head tremors, and ataxia) at 13 days post infection. Such infections may provide the basis for study of both RVF acute hepatic Disease and delayed onset encephalitic Disease in humans.
Cesar G Albarino - One of the best experts on this subject based on the ideXlab platform.
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rift valley fever virus lacking nsm proteins retains high virulence in vivo and may provide a model of human delayed onset Neurologic Disease
Virology, 2007Co-Authors: Brian H Bird, Cesar G Albarino, Stuart T NicholAbstract:Rift Valley fever virus is a significant human and veterinary pathogen responsible for explosive outbreaks throughout Africa and the Arabian Peninsula. Severe acute Disease in humans includes rapid onset hepatic Disease and hemorrhagic fever or delayed onset encephalitis. A highly efficient reverse genetics system was developed which allowed generation of recombinant RVF viruses to assess the role of NSm protein in virulence in a rat model in which wild-type RVF virus strain ZH501 (wt-ZH501) results in 100% lethal hepatic Disease 2-3 days post infection. While extensive genomic analysis indicates conservation of the NSm coding capability of diverse RVF viruses, and viruses deficient in NSs proteins are completely attenuated in vivo, comparison of wt-ZH501, a reverse genetics generated wt-ZH501 virus (R-ZH501), and R-ZH501 virus lacking the NSm proteins (R-DeltaNSm-ZH501) demonstrated that the NSm proteins were nonessential for in vivo virulence and lethality. Surprisingly, while 44% of R-DeltaNSm-ZH501 infected animals quickly developed lethal hepatic Disease similar to wt- and R-ZH501, 17% developed delayed onset Neurologic Disease (lethargy, head tremors, and ataxia) at 13 days post infection. Such infections may provide the basis for study of both RVF acute hepatic Disease and delayed onset encephalitic Disease in humans.
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rift valley fever virus lacking nsm proteins retains high virulence in vivo and may provide a model of human delayed onset Neurologic Disease
Virology, 2007Co-Authors: Brian H Bird, Cesar G Albarino, Stuart T NicholAbstract:Abstract Rift Valley fever virus is a significant human and veterinary pathogen responsible for explosive outbreaks throughout Africa and the Arabian Peninsula. Severe acute Disease in humans includes rapid onset hepatic Disease and hemorrhagic fever or delayed onset encephalitis. A highly efficient reverse genetics system was developed which allowed generation of recombinant RVF viruses to assess the role of NSm protein in virulence in a rat model in which wild-type RVF virus strain ZH501 (wt-ZH501) results in 100% lethal hepatic Disease 2–3 days post infection. While extensive genomic analysis indicates conservation of the NSm coding capability of diverse RVF viruses, and viruses deficient in NSs proteins are completely attenuated in vivo , comparison of wt-ZH501, a reverse genetics generated wt-ZH501 virus (R-ZH501), and R-ZH501 virus lacking the NSm proteins (R-ΔNSm-ZH501) demonstrated that the NSm proteins were nonessential for in vivo virulence and lethality. Surprisingly, while 44% of R-ΔNSm-ZH501 infected animals quickly developed lethal hepatic Disease similar to wt- and R-ZH501, 17% developed delayed onset Neurologic Disease (lethargy, head tremors, and ataxia) at 13 days post infection. Such infections may provide the basis for study of both RVF acute hepatic Disease and delayed onset encephalitic Disease in humans.
Elizabeth B Habermann - One of the best experts on this subject based on the ideXlab platform.
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breast cancer related paraneoplastic Neurologic Disease
Breast Cancer Research and Treatment, 2018Co-Authors: Brittany L Murphy, Nicholas L Zalewski, Amy C Degnim, Andrew Mckeon, Eoin P Flanagan, Sean J Pittock, Elizabeth B HabermannAbstract:Paraneoplastic Neurologic Disease (PND) is an aberrant immune-mediated response against the nervous system triggered by malignancy. Given the rarity, a paucity of data describing breast cancer-related PND (BC-PND) exists; we sought to further examine this specific patient population. We retrospectively identified patients at our institution from 1997 to 2016 with BC-PND. Retrospective review with a descriptive analysis determined factors associated with PND and BC, which were compared to national breast cancer median of age (61 years) and average stage at diagnosis (60% local Disease). BC-PND was diagnosed in 56 female patients at a median age of 52.8 years. Only 20% of invasive cancer patients had local Disease. The majority of patients were hormone receptor positive and Her2 negative. Neurological symptoms presented prior to BC diagnosis in 57.1% of patients. Of all patients, 30 (53.6%) had autoantibodies detected: Purkinje Cell Cytoplasmic Autoantibody Type-1 (PCA-1[anti-Yo]), n = 10; amphiphysin-IgG, n = 9; Anti-Neuronal Nuclear Autoantibody Type-2 (ANNA-2[anti-Ri]), n = 5; and others, n = 6. The most common Neurologic findings were cerebellar ataxia, myelopathy, and myopathy. Immunotherapy benefit was found to be robust (21.6%), mild to moderate (52.9%), absent (17.6%), or indeterminate (7.8%). PND symptoms often presented prior to BC diagnosis, with the BC biologic subtype characteristics typical of the general BC population. BC diagnoses were often made at younger ages than that of the general BC population and with later-stage Disease. Roughly 75% of patients benefited from immunotherapy. These data provide helpful information to providers treating this population of patients.
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breast cancer related paraneoplastic Neurologic Disease
Journal of Clinical Oncology, 2017Co-Authors: Brittany L Murphy, Nicholas L Zalewski, Amy C Degnim, Andrew Mckeon, Eoin P Flanagan, Sean J Pittock, Elizabeth B HabermannAbstract:11559Background: Paraneoplastic Neurologic Disease (PND) is an aberrant immune-mediated response against the nervous system triggered by occult malignancy. Given the rarity of this Disease, a pauci...
Donald H Gilden - One of the best experts on this subject based on the ideXlab platform.
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Herpes simplex virus-1 and varicella-zoster virus latency in ganglia
Journal of NeuroVirology, 2003Co-Authors: Bradley M. Mitchell, Donald H Gilden, Randall J Cohrs, David C Bloom, Peter G E KennedyAbstract:Two human alpha-herpesviruses, herpes simplex virus (HSV)-1 and varicella zoster virus (VZV), account for the most frequent and serious Neurologic Disease caused by any of the eight human herpesviruses. Both HSV-1 and VZV become latent in ganglia. In this review, the authors describe features of latency for these viruses, such as distribution, prevalence, abundance, and configuration of viral DNA in latently infected human ganglia, as well as transcription, translation, and cell type infected. Studies of viral latency in animal models are also discussed. For each virus, remaining questions and future studies to understand the mechanism of latency are discussed with respect to prevention of serious cutaneous, ocular, and Neurologic Disease produced by virus reactivation.
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the value of cerebrospinal fluid antiviral antibody in the diagnosis of Neurologic Disease produced by varicella zoster virus
Journal of the Neurological Sciences, 1998Co-Authors: Donald H Gilden, Jeffrey L Bennett, B K Kleinschmidtdemasters, D D Song, A S Yee, I SteinerAbstract:We studied four patients with subacute to chronic varicella zoster virus (VZV) infection of the central nervous system (CNS). VZV infection was verified by detecting antibody to VZV in the cerebrospinal fluid (CSF). VZV caused myelitis in two patients and encephalitis in two patients. In one of the patients with VZV encephalitis, in addition to VZV IgM antibody, VZV DNA was found in the CSF. Among the four patients with VZV infection of the CNS, CSF antibody to VZV was the crucial diagnostic laboratory test which corroborated the clinical features, and indicated that VZV caused Neurologic Disease. In addition to looking for amplifiable VZV DNA in the CSF of patients with Neurologic Disease whose clinical and radiologic features suggest VZV infection, we also recommend a search for CSF antibody to VZV, particularly in patients with intervals of weeks to months between zoster and the onset of Neurologic Disease, or in those patients without rash in whom the tempo of illness is unknown.
