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Lack of Correlation between Neutralizing Antibody Production and Suppression of Coxsackievirus B-3 Replication in Target Organs: Evidence for Involvement of Mononuclear Inflammatory Cells in Host Defense¹

From the Department of Pathology, Cornell University Medical College, New York, New York 10021

Abstract

CD-1 mice inoculated with coxsackievirus B-3 i.p. developed a generalized infection involving the heart, pancreas, and liver. The disease was nonlethal and viral growth in the target organs was terminated in about a week. Administration of cortisone acetate 30 min to 2 hr before infection markedly enhanced the severity of disease. Abnormally high titers of virus were found in the target organs between days 3 and 7 with persistence of infectious virus in the heart for at least 2 weeks. In addition the extent of necrosis of myofibers, pancreatic acini, and hepatic parenchyma was increased and a high percentage of the animals died. There was no evidence that the anti-viral antibody response was impaired in steroid-treated mice since concentrations of neutralizing antibody in the circulation were normal. In contrast, immigration of mononuclear inflammatory cells into the hearts of these animals was depressed and when present, foci of inflammation contained some polymorphonuclear leukocytes. The data indicate that inhibition of coxsackieviral growth cannot be attributed to the sole effects of neutralizing antibody and suggest that mononuclear inflammatory cells infiltrating the heart play a role in primary host defense.

Footnotes

¹ This work was supported in part by Grant-in-Aid 77-1081 from the American Heart Association and National Institutes of Health Grant HL-17404.

² Preceptor, New York Heart Association.

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