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Benign human enterovirus becomes virulent in selenium-deficient mice
M A Beck1, P C Kolbeck, L H Rohr
1Frank Porter Graham Child Development Center, University of North Carolina, Chapel Hill.
Journal of Medical Virology
|June 1, 1994
Summary
Selenium deficiency exacerbates coxsackievirus B3 heart damage in mice. Viral mutations in deficient hosts increase cardiac pathology, highlighting the impact of nutritional status on viral infection severity.
Area of Science:
- Virology
- Nutritional Science
- Cardiology
Background:
- Keshan disease is a selenium-responsive cardiomyopathy potentially linked to coxsackieviruses.
- Amyocarditic coxsackievirus B3 (CVB3/0) typically does not cause heart pathology in selenium-adequate hosts.
Purpose of the Study:
- To investigate the role of host selenium status in coxsackievirus B3-induced cardiac pathology.
- To determine if viral adaptation occurs in selenium-deficient hosts.
Main Methods:
- Inoculation of selenium-adequate and selenium-deficient mice with an amyocarditic strain of coxsackievirus B3 (CVB3/0).
- Assessment of cardiac pathology in infected mice.
- Recovery and re-inoculation of virus from infected mice into naive hosts.
Main Results:
- Selenium-deficient mice developed extensive cardiac pathology when infected with CVB3/0, unlike selenium-adequate controls.
- Virus recovered from selenium-deficient mice induced significant heart damage in selenium-adequate mice, indicating viral mutation.
- Host nutritional status significantly influences the severity of coxsackievirus-induced heart disease.
Conclusions:
- Selenium deficiency is a critical factor in the development of coxsackievirus-induced cardiomyopathy.
- Coxsackievirus B3 can adapt and become virulent in selenium-deficient hosts.
- Host nutritional status plays a crucial role in modulating viral pathogenicity.