Why the study?
Does a selenium-deficient host environment increase the virulence of Coxsackievirus B3 and the severity of resulting myocarditis in a mouse model?
Does a selenium-deficient host environment increase the virulence of Coxsackievirus B3 and the severity of resulting myocarditis in a mouse model?
Replication of Coxsackievirus B3 in a selenium-deficient host induces a phenotypic change in the virus that increases its virulence and the severity of subsequent myocarditis.
Answers are grounded in this paper and cite their sources.
Indicates Se deficiency can drive CVB3 virulence in mice; hypothesis-generating for human myocarditis risk.
Coxsackievirus B3 (CVB3/20)-induced myocarditic lesions occurred more quickly and were more severe and virus titers in heart and liver were higher in selenium (Se)-deficient than Se-adequate mice. NK cell activity and serum neutralizing antibody titers were similar in both Se-adequate and -deficient CVB3/20-infected mice; however, lymphocyte proliferation to both mitogen and antigen was decreased in Se-deficient mice. CVB3/20 isolated from Se-deficient donor mice and inoculated into Se-adequate recipient mice induced severe myocarditis. In contrast, CVB3/20 isolated from Se-adequate donor mice and inoculated into Se-adequate recipient mice induced only moderate myocarditis, similar to that caused by the original virus stock. Thus, the general population of CVB3/20 virions, as a consequence of replicating in an Se-deficient host, underwent a phenotypic change to increased virulence. These results have important implications for the emergence of virulent viruses.
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Beck et al. (1994) studied this question.
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