Benign human enterovirus becomes virulent in selenium-deficient mice.
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.
Beck
M A
MA
Frank Porter Graham Child Development Center, University of North Carolina, Chapel Hill.
Kolbeck
P C
PC
Rohr
L H
LH
Shi
Q
Q
Morris
V C
VC
Levander
O A
OA
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
D012643:Selenium