wt measles SSPE - DISPATCHES W ild-type Measles Virus in...

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Wild-type Measles Virus in Brain Tissue of Children with Subacute Sclerosing Panencephalitis, Argentina Paola Roxana Barrero,* Jorge Grippo,* Mariana Viegas,* and Alicia Susana Mistchenko* We studied eight children who had measles at 6 to 10 months of age during the 1998 Argentine measles outbreak and in whom subacute sclerosing panencephalitis devel- oped 4 years later. We report the genetic characterization of brain tissue–associated measles virus samples from three patients. Phylogenetic relationships clustered these viruses with the wild-type D6 genotype isolated during the 1998 outbreak. The children received measles vaccine; however, vaccinal strains were not found. M easles is often incorrectly regarded as a mild disease, and priority is not given to measles elimination pro- grams in some countries (1). Nevertheless, substantial progress has been made in eliminating measles virus from the Americas through massive vaccination campaigns and maintaining high measles population immunity over time. From 1990 to 1996, measles cases declined from 250,000 to 2,109; however, in 1997, measles reemerged in the Americas, with 70,983 confirmed cases. From the last Argentine outbreak (July 1997–May 1999), 10,354 con- firmed measles cases were reported, most of them in unvaccinated preschool-aged children in the greater Buenos Aires metropolitan area (2). Although measles virus ( Morbillivirus genus, Paramyxovirus family) is not highly neurotropic, it can establish long-term persistent infection in brain cells. Three different neurologic complications result from inter- actions of measles virus with neural tissue. Acute postin- fectious encephalitis, usually appearing 5–14 days after the rash, is thought to be a virus-induced autoimmune disease. Measles inclusion–body encephalitis, which occurs in immunocompromised patients after a latent period of 3–6 months, is believed to be a direct measles virus infection of neural tissue. The third form, subacute sclerosing panen- cephalitis (SSPE), manifests 2–10 years after primary measles infection as a progressive and fatal chronic neu- rodegenerative disease caused by persistent defective measles virus in neurons and oligodendrocytes. SSPE develops with high titers of anti-measles antibodies both in cerebrospinal fluid (CSF) and serum, which seem unable to eliminate measles virus from the brain (3). Although measles virus is serologically monotypic, genetic variability has defined eight clades, including 20 genotypes and a putative new genotype that are geograph- ically and temporally restricted (4). Evidence does not indicate that wild-type measles virus strains differ in terms of either pathogenesis or neurovirulence. Measles virus recovered from patients with SSPE differs from wild-type viruses in a number of mutations that mainly affect the matrix, hemagglutinin (H), nucleocapsid (N), and fusion genes. The matrix accumulates the highest level of muta- tions in the entire open reading frame; by contrast, the N is
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This note was uploaded on 07/12/2011 for the course BIO 620 taught by Professor Hardy during the Spring '11 term at University of Florida.

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wt measles SSPE - DISPATCHES W ild-type Measles Virus in...

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