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Träfflista för sökning "WFRF:(Skoldenberg B) "

Sökning: WFRF:(Skoldenberg B)

  • Resultat 1-10 av 24
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1.
  • Abdelmagid, N., et al. (författare)
  • The Calcitonin Receptor Gene Is a Candidate for Regulation of Susceptibility to Herpes simplex Type 1 Neuronal Infection Leading to Encephalitis in Rat
  • 2012
  • Ingår i: Plos Pathogens. - : Public Library of Science (PLoS). - 1553-7374. ; 8:6
  • Tidskriftsartikel (refereegranskat)abstract
    • Herpes simplex encephalitis (HSE) is a fatal infection of the central nervous system (CNS) predominantly caused by Herpes simplex virus type 1. Factors regulating the susceptibility to HSE are still largely unknown. To identify host gene(s) regulating HSE susceptibility we performed a genome-wide linkage scan in an intercross between the susceptible DA and the resistant PVG rat. We found one major quantitative trait locus (QTL), Hse1, on rat chromosome 4 (confidence interval 24.3-31 Mb; LOD score 29.5) governing disease susceptibility. Fine mapping of Hse1 using recombinants, haplotype mapping and sequencing, as well as expression analysis of all genes in the interval identified the calcitonin receptor gene (Calcr) as the main candidate, which also is supported by functional studies. Thus, using unbiased genetic approach variability in Calcr was identified as potentially critical for infection and viral spread to the CNS and subsequent HSE development.
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  • Abdelmagid, N., et al. (författare)
  • Von Willebrand Factor Gene Variants Associate with Herpes simplex Encephalitis
  • 2016
  • Ingår i: Plos One. - : Public Library of Science (PLoS). - 1932-6203. ; 11:5
  • Tidskriftsartikel (refereegranskat)abstract
    • Herpes simplex encephalitis (HSE) is a rare complication of Herpes simplex virus type-1 infection. It results in severe parenchymal damage in the brain. Although viral latency in neurons is very common in the population, it remains unclear why certain individuals develop HSE. Here we explore potential host genetic variants predisposing to HSE. In order to investigate this we used a rat HSE model comparing the HSE susceptible SHR (Spontaneously Hypertensive Rats) with the asymptomatic infection of BN (Brown Norway). Notably, both strains have HSV-1 spread to the CNS at four days after infection. A genome wide linkage analysis of 29 infected HXB/BXH RILs (recombinant inbred lines-generated from the prior two strains), displayed variable susceptibility to HSE enabling the definition of a significant QTL (quantitative trait locus) named Hse6 towards the end of chromosome 4 (160.89-174Mb) containing the Vwf (von Willebrand factor) gene. This was the only gene in the QTL with both cis-regulation in the brain and included several non-synonymous SNPs (single nucleotide polymorphism). Intriguingly, in human chromosome 12 several SNPs within the intronic region between exon 43 and 44 of the VWF gene were associated with human HSE pathogenesis. In particular, rs917859 is nominally associated with an odds ratio of 1.5 (95% CI 1.11-2.02; p-value = 0.008) after genotyping in 115 HSE cases and 428 controls. Although there are possibly several genetic and environmental factors involved in development of HSE, our study identifies variants of the VWF gene as candidates for susceptibility in experimental and human HSE.
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  • Gnann, J. W., et al. (författare)
  • Herpes Simplex Encephalitis: Lack of Clinical Benefit of Long-term Valacyclovir Therapy
  • 2015
  • Ingår i: Clinical Infectious Diseases. - : Oxford University Press (OUP). - 1058-4838 .- 1537-6591. ; 61:5, s. 683-691
  • Tidskriftsartikel (refereegranskat)abstract
    • Background. Despite the proven efficacy of acyclovir (ACV) therapy, herpes simplex encephalitis (HSE) continues to cause substantial morbidity and mortality. Among patients with HSE treated with ACV, the mortality rate is approximately 14%-19%. Among survivors, 45%-60% have neuropsychological sequelae at 1 year. Thus, improving therapeutic approaches to HSE remains a high priority. Methods. Following completion of a standard course of intravenous ACV, 87 adult patients with HSE (confirmed by positive polymerase chain reaction [PCR] for herpes simplex virus DNA in cerebrospinal fluid) were randomized to receive either valacyclovir (VACV) 2 g thrice daily (n = 40) or placebo tablets (n = 47) for 90 days (12 tablets of study medication daily). The primary endpoint was survival with no or mild neuropsychological impairment at 12 months, as measured by the Mattis Dementia Rating Scale (MDRS). Logistic regression was utilized to assess factors related to the primary endpoint. Results. The demographic characteristics of the 2 randomization groups were statistically similar with no significant differences in age, sex, or race. At 12 months, there was no significant difference in the MDRS scoring for VACV-treated vs placebo recipients, with 85.7% and 90.2%, respectively, of patients demonstrating no or mild neuropsychological impairment (P = .72). No significant study-related adverse events were encountered in either treatment group. Conclusions. Following standard treatment with intravenous ACV for PCR-confirmed HSE, an additional 3-month course of oral VACV therapy did not provide added benefit as measured by neuropsychological testing 12 months later in a population of relatively high-functioning survivors.
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  • Hjalmarsson, A, et al. (författare)
  • Encephalitis after influenza in Sweden 1987-1998: a rare complication of a common infection
  • 2009
  • Ingår i: European neurology. - : S. Karger AG. - 1421-9913 .- 0014-3022. ; 61:5, s. 289-294
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim of this study was to investigate the incidence of influenza-related encephalitis in Sweden during 11.5 years. Studies from Japan report an increased incidence of influenza-related encephalitis/encephalopathy. Few other studies are available. We conducted a retrospective register-based study on the Swedish National Inpatient Register, which covers all Swedish hospitals. In 1987–1998, a total number of 14,250 hospitalized individuals had an influenza diagnosis (population incidence: 137 per million personyears). In-hospital mortality was 4.1%. Using three different approaches, only 21 cases of influenza-related encephalitis were found, corresponding to a rate of 1.5 per 1,000 hospitalized persons with an influenza diagnosis (population incidence 0.21 per million person-years). We conclude that encephalitis following influenza occurs rarely, or is an infrequently recognized, diagnosed or reported complication. The cases we studied in detail have all recovered without sequels.
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