Why the study?
Does coxsackie B3 virus infection alter blood amino acid levels and correlate with viral titers and histopathology in mice?
Does coxsackie B3 virus infection alter blood amino acid levels and correlate with viral titers and histopathology in mice?
Coxsackie B3 virus infection in mice causes early and persistent depression of blood amino acids, suggesting that maintaining optimal nutrition during acute infection may help sustain the host's anabolic response.
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Hypothesis-generating in murine coxsackie B3 myocarditis; leaves open any nutritional intervention in human viral myocarditis.
Mice, 14–16 days old, were challenged with coxsackie B3 virus to define and ascertain possible mechanisms for changes in amino acids in blood accompanying infection with this virus and to correlate amino-acid responses with viral titers in blood and myocardium and with gross and histopathologic evidence of disease. There was significant depression of total concentration of amino acids in blood and profound depression of amino acids important for protein synthesis 15 min after challenge; these changes persisted through day 5. Viremia was detectable from 15 min to day 6 after challenge. Myocardial virus persisted until day 10. Weights of infected animals were depressed on days 5 through 12, but compensatory growth was noted subsequently. Gross myocardial lesions were present in 50% of mice three months after challenge. These findings suggest that maintenance of optimal nutrition during acute infection may be important in sustaining the early anabolic response of the host and can prevent the decreased rate of growth.
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Feigin et al. (1972) studied this question.
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