title: Benign human enterovirus becomes virulent in selenium-deficient mice.
abstract: Coxsackieviruses have been implicated as possible co-factors in the etiology of the selenium (Se)-responsive cardiomyopathy known as Keshan disease. Here we report that a cloned and sequenced amyocarditic coxsackievirus B3 (CVB3/0), which causes no pathology in the hearts of Se-adequate mice, induces extensive cardiac pathology in Se-deficient mice. CVB3/0 recovered from the hearts of Se-deficient mice inoculated into Se-adequate mice induced significant heart damage, suggesting mutation of the virus to a virulent genotype. We demonstrate the important role of host nutritional status in determining the severity of a viral infection.
authors.affiliation: Frank Porter Graham Child Development Center, University of North Carolina, Chapel Hill.
authors.forename: M A
authors.initials: MA
authors.lastname: Beck
authors.forename: P C
authors.initials: PC
authors.lastname: Kolbeck
authors.forename: L H
authors.initials: LH
authors.lastname: Rohr
authors.forename: Q
authors.initials: Q
authors.lastname: Shi
authors.forename: V C
authors.initials: VC
authors.lastname: Morris
authors.forename: O A
authors.initials: OA
authors.lastname: Levander
mesh_terms: D000818:Animals; D003384:Coxsackievirus Infections / Q000382:microbiology*; D029822:Enterovirus B, Human / Q000472:pathogenicity*; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D009205:Myocarditis / Q000382:microbiology*; D012643:Selenium / Q000172:deficiency*; D014774:Virulence / Q000235:genetics
chemical_list: D012643:Selenium