Host nutritional selenium status as a driving force for influenza virus mutations 1 HEATHER K. NELSON * , QING SHI † , PETER VAN DAEL ‡ , EDUARDO J. SCHIFFRIN ‡ , STEPHANIE BLUM ‡ , DENIS BARCLAY ‡ , ORVILLE A. LEVANDER § and MELINDA A. BECK * ,† 2 Departments of * Nutrition and † Pediatrics 2 , University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7220, USA; ‡ Nestlé Research Center, Lausanne, Switzerland; and § USDA, ARS, Beltsville Human Nutrition Research Center, Beltsville, Maryland 2 Correspondence: Department of Pediatrics, 535 Burnett-Womack, CB #7220, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7220, USA. E-mail: melinda_beck@unc.edu <h3>SPECIFIC AIM</h3> To determine whether host selenium (Se) deficiency can induce changes in the genome of a replicating influenza virus such that a normally mild virus converts into a more virulent strain and to characterize such genomic changes. <h3>PRINCIPAL FINDINGS</h3> <h3>1. Replication of a mild strain of influenza virus in Se-deficient mice results in a novel virulent strain that causes severe lung pathology even when passed into Se-adequate mice</h3> Se-deficient mice developed much more severe lung pathology postinfection with influenza virus than Se-adequate infected mice.
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Host nutritional selenium status as a driving force for influenza virus mutations
NELSON, HEATHER K.; SHI, QING; VAN DAEL, PETER; SCHIFFRIN, EDUARDO J.; BLUM, STEPHANIE; BARCLAY, DENIS; LEVANDER, ORVILLE A.; BECK, MELINDA A.
Follow The FASEB Journal
, Volume 15 (10): 1846
Fed of American Socs for Experimental Biology – Aug 1, 2001
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