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Angela Vincent - One of the best experts on this subject based on the ideXlab platform.
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pediatric herpes simplex Virus Encephalitis complicated by n methyl d aspartate receptor antibody Encephalitis
Journal of the Pediatric Infectious Diseases Society, 2015Co-Authors: Alasdair Bamford, Yael Hacohen, Angela Vincent, Belinda H A Crowe, Antonia Clarke, Gareth Tudorwilliams, Vanessa Sanchoshimizu, Sunil PullaperumaAbstract:: N-methyl-D-aspartate receptor antibodies (NMDAR-Abs) can contribute to neurological relapse after herpes simplex Virus Encephalitis (HSE). We describe a child with NMDAR-Ab Encephalitis after HSE, which was recognized and treated early. We discuss the case in the context of existing reports, and we propose a modified immunotherapy strategy to minimize risk of viral reactivation.
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n methyl d aspartate receptor antibodies in post herpes simplex Virus Encephalitis neurological relapse
Movement Disorders, 2014Co-Authors: Yael Hacohen, Kumaran Deiva, Phillipa Pettingill, Esse Menson, Pascale Chretien, Patrick Waters, Ata Siddiqui, Marc Tardieu, Angela VincentAbstract:Herpes simplex Virus Encephalitis (HSVE) is a devastating condition that relapses, often with a chorea in children, despite adequate antiviral treatment. At relapse, evidence of viral replication is frequently absent, suggesting that the relapse may be immune-mediated. Seven children who had a neurological relapse following their initial Encephalitis, identified from 20 cases of pediatric HSVE, were studied. Serum and/or cerebrospinal fluid (CSF) were tested for N-methyl-D-aspartate receptor (NMDAR) and other antibodies previously reported in central nervous system autoimmunity. Five of the 7 relapsing children had choreoathetosis; 2 of these were NMDAR antibody-positive, 2 were negative (1 with HSV-positive CSF), and 1 was not available for testing. An additional patient, who relapsed with cognitive regression but with no movement disorder, was also NMDAR antibody-positive. In 2 of the NMDAR antibody-positive patients who were treated at relapse and in 1 who was treated only after 10 years of having a relaps- ing encephalopathy, a beneficial response was observed. Neurological relapses after HSVE may frequently be immune-mediated, particularly in children with chorea. NMDAR antibodies are common, and immunotherapy may be beneficial. V C 2013 International Parkinson and Move- ment Disorder Society. Key W ords: herpes simplex Virus; Encephalitis; N-methyl-D-aspartate (NMDA) receptor; choreoatheto- sis; movement disorder; relapsing
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n methyl d aspartate receptor antibodies in post herpes simplex Virus Encephalitis neurological relapse
Movement Disorders, 2014Co-Authors: Yael Hacohen, Kumaran Deiva, Phillipa Pettingill, Esse Menson, Pascale Chretien, Patrick Waters, Ata Siddiqui, Marc Tardieu, Jeanpierre Lin, Angela VincentAbstract:Herpes simplex Virus Encephalitis (HSVE) is a devastating condition that relapses, often with a chorea in children, despite adequate antiviral treatment. At relapse, evidence of viral replication is frequently absent, suggesting that the relapse may be immune-mediated. Seven children who had a neurological relapse following their initial Encephalitis, identified from 20 cases of pediatric HSVE, were studied. Serum and/or cerebrospinal fluid (CSF) were tested for N-methyl-D-aspartate receptor (NMDAR) and other antibodies previously reported in central nervous system autoimmunity. Five of the 7 relapsing children had choreoathetosis; 2 of these were NMDAR antibody-positive, 2 were negative (1 with HSV-positive CSF), and 1 was not available for testing. An additional patient, who relapsed with cognitive regression but with no movement disorder, was also NMDAR antibody-positive. In 2 of the NMDAR antibody-positive patients who were treated at relapse and in 1 who was treated only after 10 years of having a relapsing encephalopathy, a beneficial response was observed. Neurological relapses after HSVE may frequently be immune-mediated, particularly in children with chorea. NMDAR antibodies are common, and immunotherapy may be beneficial.
Yael Hacohen - One of the best experts on this subject based on the ideXlab platform.
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pediatric herpes simplex Virus Encephalitis complicated by n methyl d aspartate receptor antibody Encephalitis
Journal of the Pediatric Infectious Diseases Society, 2015Co-Authors: Alasdair Bamford, Yael Hacohen, Angela Vincent, Belinda H A Crowe, Antonia Clarke, Gareth Tudorwilliams, Vanessa Sanchoshimizu, Sunil PullaperumaAbstract:: N-methyl-D-aspartate receptor antibodies (NMDAR-Abs) can contribute to neurological relapse after herpes simplex Virus Encephalitis (HSE). We describe a child with NMDAR-Ab Encephalitis after HSE, which was recognized and treated early. We discuss the case in the context of existing reports, and we propose a modified immunotherapy strategy to minimize risk of viral reactivation.
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n methyl d aspartate receptor antibodies in post herpes simplex Virus Encephalitis neurological relapse
Movement Disorders, 2014Co-Authors: Yael Hacohen, Kumaran Deiva, Phillipa Pettingill, Esse Menson, Pascale Chretien, Patrick Waters, Ata Siddiqui, Marc Tardieu, Angela VincentAbstract:Herpes simplex Virus Encephalitis (HSVE) is a devastating condition that relapses, often with a chorea in children, despite adequate antiviral treatment. At relapse, evidence of viral replication is frequently absent, suggesting that the relapse may be immune-mediated. Seven children who had a neurological relapse following their initial Encephalitis, identified from 20 cases of pediatric HSVE, were studied. Serum and/or cerebrospinal fluid (CSF) were tested for N-methyl-D-aspartate receptor (NMDAR) and other antibodies previously reported in central nervous system autoimmunity. Five of the 7 relapsing children had choreoathetosis; 2 of these were NMDAR antibody-positive, 2 were negative (1 with HSV-positive CSF), and 1 was not available for testing. An additional patient, who relapsed with cognitive regression but with no movement disorder, was also NMDAR antibody-positive. In 2 of the NMDAR antibody-positive patients who were treated at relapse and in 1 who was treated only after 10 years of having a relaps- ing encephalopathy, a beneficial response was observed. Neurological relapses after HSVE may frequently be immune-mediated, particularly in children with chorea. NMDAR antibodies are common, and immunotherapy may be beneficial. V C 2013 International Parkinson and Move- ment Disorder Society. Key W ords: herpes simplex Virus; Encephalitis; N-methyl-D-aspartate (NMDA) receptor; choreoatheto- sis; movement disorder; relapsing
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n methyl d aspartate receptor antibodies in post herpes simplex Virus Encephalitis neurological relapse
Movement Disorders, 2014Co-Authors: Yael Hacohen, Kumaran Deiva, Phillipa Pettingill, Esse Menson, Pascale Chretien, Patrick Waters, Ata Siddiqui, Marc Tardieu, Jeanpierre Lin, Angela VincentAbstract:Herpes simplex Virus Encephalitis (HSVE) is a devastating condition that relapses, often with a chorea in children, despite adequate antiviral treatment. At relapse, evidence of viral replication is frequently absent, suggesting that the relapse may be immune-mediated. Seven children who had a neurological relapse following their initial Encephalitis, identified from 20 cases of pediatric HSVE, were studied. Serum and/or cerebrospinal fluid (CSF) were tested for N-methyl-D-aspartate receptor (NMDAR) and other antibodies previously reported in central nervous system autoimmunity. Five of the 7 relapsing children had choreoathetosis; 2 of these were NMDAR antibody-positive, 2 were negative (1 with HSV-positive CSF), and 1 was not available for testing. An additional patient, who relapsed with cognitive regression but with no movement disorder, was also NMDAR antibody-positive. In 2 of the NMDAR antibody-positive patients who were treated at relapse and in 1 who was treated only after 10 years of having a relapsing encephalopathy, a beneficial response was observed. Neurological relapses after HSVE may frequently be immune-mediated, particularly in children with chorea. NMDAR antibodies are common, and immunotherapy may be beneficial.
John K Fazakerley - One of the best experts on this subject based on the ideXlab platform.
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in semliki forest Virus Encephalitis antibody rapidly clears infectious Virus and is required to eliminate viral material from the brain but is not required to generate lesions of demyelination
Journal of General Virology, 2008Co-Authors: Rennos Fragkoudis, Catherine M Ballany, Amanda Boyd, John K FazakerleyAbstract:Semliki Forest Virus (SFV) infection of the laboratory mouse provides a well-characterized tractable system to study the pathogenesis of Virus Encephalitis and Virus induced demyelination. In microMT mice, which have no antibodies, infectious Virus persisted in both the serum and the brain for several weeks, indicating that antibodies are required to eliminate infectious Virus. In immunocompetent mice, Virus infectivity in the brain was undetectable after the first week of infection, but Virus RNA levels declined slowly. Following SFV infection, lesions of demyelination were present in the brains of both immunocompetent and microMT mice, indicating that antibodies are not required to generate lesions of demyelination.
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pathogenesis of semliki forest Virus Encephalitis
Journal of NeuroVirology, 2002Co-Authors: John K FazakerleyAbstract:This article provides a review of the pathogenesis of Semliki Forest Virus (SFV) Encephalitis. In mice, outcome of infection varies according to age of the mouse and strain of the Virus and can include acute Encephalitis, subacute demyelinating meningoencephalomyelitis, and persistent subclinical central nervous system (CNS) infection. All strains of Virus are virulent in mice infected 14 days age, whereas the A7(74) strain is avirulent. The genetic difference between these strains maps to the nsp3 gene. For A7(74) Virus, age-related virulence correlates with ability of CNS neurons to replicate Virus and undergo apoptotic cell death. Immature developing neurons support complete Virus replication but as neuronal populations and circuits mature in the postnatal brain, Virus infection becomes progressively restricted and nonproductive. This restricted replication can be overcome by gold I compounds, which may function by inducing neuronal dedifferentiation to a state permissive for Virus replication. Biochemical pathways associated with membrane biogenesis may be an important determinant of this effect. Infection of some developing neuronal populations results in apoptosis, whereas infection of mature neurons results in persistent infection. An active type-I interferon system prevents Virus spread in extraneural tissues. An initial high-titer plasma viremia is controlled by immunoglobulin M (IgM) antibodies. Virus enters the brain across cerebral endothelial cells and initiates scattered foci of perivascular infection. The blood-brain barrier is disrupted. Neurons and oligodendrocytes are the cell types most frequently infected. Infectivity in the brain can be eliminated by IgG antibodies, though an active T-cell response is required for Virus elimination. Lesions of inflammatory demyelination require the presence of CD8 + T lymphocytes and probably result from destruction by these cells of virally infected oligodendrocytes. Journal of NeuroVirology (2002) 8(suppl. 2), 66‐74.
Steven Sonnesyn - One of the best experts on this subject based on the ideXlab platform.
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Powassan Virus Encephalitis,
2013Co-Authors: Justin Birge, Steven SonnesynAbstract:Powassan Virus (POWV) is a rare tick-borne agent of Encephalitis in North America. Historically, confi rmed cases occurred mainly in the northeastern United States. Since 2008, confi rmed cases in Minnesota and Wisconsin have increased. We report a fatal case of POWV Encephalitis in Minnesota. POWV infection should be suspected in tickexposed patients with viral Encephalitis, Case Report A 67-year-old woman from Aitkin, Minnesota, USA, sought treatment at a local hospital on May 30, 2011, with a 3-day history of dizziness, fever of up to 103°F (39.4°C), chills, malaise, nausea, and occasional confusion with slurred speech. She had no respiratory or gastrointestinal symptoms and no history of ill contacts, travel, environmental exposures, or other recent illness. She had not been exposed to animals or vectors, other than those endemic to her area of residence, which included mosquitoes and deer ticks. She had removed many deer ticks after gardening or hiking in the woods. The patient’s past medical history was notable for colon cancer, which had been treated with a partial colectomy in October 2010 and chemotherapy through April 2011. She also had a history of hypertension, cutaneous lupus, and a remote cerebral aneurysm with surgical clipping. Medications she was taking were atenolol, hydroxychloroquine, and valsartan. On admission, the woman was alert and reported mild neck tenderness. Her temperature was 100°F (37.8°C), blood pressure 138/77 mm Hg, pulse rate 83 beats/min, respiratory rate 22 breaths/min, and oxygen saturation 98 % on room air. Results of neurologic, cardiac, and respiratory examinations were normal. Studies with normal test results included comprehensive metabolic panel, urinalysis, computed tomographic scan of the head, and chest radiograph. Results of serum screen for Borrelia burgdorferi antibodies (by ELISA) were negative. Leukocyte count was within reference range (10.8 × 10 3 /mm 3), with neutrophil (polymorphonuclear leukocytes) predominance (80%). Her cerebrospinal fluid (CSF) showed 80 leukocytes (89 % polymorphonuclea
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Powassan Virus Encephalitis, Minnesota, USA
Emerging infectious diseases, 2012Co-Authors: Justin R Birge, Steven SonnesynAbstract:Powassan Virus (POWV) is a rare tick-borne agent of Encephalitis in North America. Historically, confirmed cases occurred mainly in the northeastern United States. Since 2008, confirmed cases in Minnesota and Wisconsin have increased. We report a fatal case of POWV Encephalitis in Minnesota. POWV infection should be suspected in tick-exposed patients with viral Encephalitis.
Kirk E. Smith - One of the best experts on this subject based on the ideXlab platform.
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Powassan Virus Encephalitis, Minnesota, USA
Emerging infectious diseases, 2013Co-Authors: David F. Neitzel, Ruth Lynfield, Kirk E. SmithAbstract:To the Editor: Birge and Sonnesyn report the first death of a Minnesota resident caused by Powassan Virus (POWV) (1). However, they provide an inaccurate description of several critical diagnostic and surveillance issues concerning POWV. The 17 POWV infections detected in Minnesota residents from 2008 through 2011 (6 cases were identified through 2010, not 8 as reported by Birge and Sonnesyn) (Minnesota Department of Health [MDH], unpub. data) were found through enhanced surveillance. Health alerts to Minnesota medical providers described POWV as a possible etiologic agent for viral meningitis and Encephalitis. Providers consulted with MDH on suspected cases and submitted serum and cerebrospinal fluid specimens to MDH. MDH conducted serologic testing for endemic arboViruses (including POWV) and reverse transcription PCR (RT-PCR) for flaviViruses and POWV. MDH would not have detected any POWV infections without enhanced surveillance. Limited field studies also identified POWV-infected ticks in 4 Minnesota counties (not 2 as reported [1]) (MDH, unpub. data). Commercial laboratories do not provide testing for POWV, and only a few state health department laboratories and the Centers for Disease Control and Prevention offer testing. Serologic testing (enzyme immunoassay with plaque-reduction neutralization testing confirmation) is preferred (2) because POWV RT-PCRs are not validated, and the short viremic periods of flaviViruses limit their usefulness (3). Few POWV infections are identified by lineage (prototype vs. deer tick Virus); Minnesota’s first case in 2008 was identified as a deer tick Virus infection, but the lineage was unknown for the other 16 cases. However, many case-patients had likely exposure to Ixodes scapularis ticks (blacklegged ticks), the tick species associated with deer tick Virus transmission, and Viruses from all POWV-positive tick pools were confirmed as deer tick Virus by sequencing. The distribution of the 2 lineages in North America is poorly understood, and most cases likely go undetected without specific POWV surveillance efforts.
