Background: Vitiligo is an autoimmune disease resulting in skin depigmentation. Treatment options are limited.
Objectives: To examine disease burden and healthcare resource utilization (HCRU) among patients with vitiligo in Québec, Canada.
There is limited understanding on healthcare utilization and costs of age-related comorbidities such as cardiovascular, bone and renal disease/disorder in people living with human immunodeficiency virus, so we compared comorbidity prevalence and associated healthcare utilization and costs. Through the Quebec health insurance database, people living with human immunodeficiency virus on antiretroviral therapy for ≥6 months from January 2006 to June 2012 were categorized by their comorbidity status using International Classification of Diseases (ICD)-9 codes, and controls without human immunodeficiency virus diagnosis or antiretroviral therapy use were age and gender matched. We compared healthcare utilization and costs.
View Article and Find Full Text PDFThe ordered copolymerization of viral proteins to form the herpes simplex virus (HSV) capsid occurs within the nucleus of the infected cell and is a complex process involving the products of at least six viral genes. In common with capsid assembly in double-stranded DNA bacteriophages, HSV capsid assembly proceeds via the assembly of an outer capsid shell around an interior scaffold. This capsid intermediate matures through loss of the scaffold and packaging of the viral genomic DNA.
View Article and Find Full Text PDFSpontaneous null mutations represent low frequency events that irreversibly and completely inactivate a gene, and can often consist of major gene alterations. To study the molecular mechanisms leading to recessive spontaneous null mutations in the human genome, we designed and tested a selection procedure in cell culture to enrich for this rare class of spontaneous mutations. The KT cell line contains the herpes simplex virus type 1 (HSV-1) thymidine kinase (tk) gene and the neomycin-resistance gene (neo), from plasmid pSV2neoKT, integrated as a single-copy in the human tk- cell line 143B.
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