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Generation of Cytotoxic T Lymphocytes during Coxsackievirus B-3 Infection

I. Model and Viral Specificity¹

From the Department of Pathology, Cornell University Medical College, New York, New York 10021, and the Department of Microbiology and Immunology, SUNY, Downstate Medical Center, Brooklyn, New York 11203

Abstract

The production of cytotoxic cells in the spleens of adult male BALB/c mice infected with Coxsackievirus B-3 has been examined. An in vitro ⁵¹Cr release assay was used to measure cytotoxic activity against virus-infected and uninfected neonatal syngeneic fibroblasts. Cytotoxicity of immune spleen cells against virus-infected targets was detected on the 3rd day after infection, reached a peak on day 7, and then declined to low levels by days 12 and 14. Spleen cells obtained 3 and 5 days after infection also exerted cytotoxicity against uninfected fibroblasts, but by the 7th day there was little or no reactivity against uninfected target cells, although activity against infected fibroblasts was maximal at this time. Reciprocal assays performed by using Coxsackie and vaccinia viruses provided evidence of virus specificity of the cytotoxic reaction. When spleen cells were obtained 7 days after infection, the Coxsackievirus-immune population was not cytotoxic for vaccinia-infected fibroblasts, and the vaccinia-immune population was not cytotoxic for Coxsackievirus-infected targets, although each immune cell preparation caused significant lysis of fibroblasts infected with the homologous virus. Additional studies showed that primary mouse or hyperimmune rabbit anti-Coxsackieviral serum could not block immune spleen cell cytotoxicity or induce complement-mediated lysis of in fected targets. The findings indicate that Coxsackievirus infection results in surface membrane alterations, but no evidence was obtained that antiviral antibody could react with the infected cells.

Footnotes

¹ This work was supported by National Institutes of Health Grants HL-17404 and TO1-GM-00078 and by Grant-in-Aid 74-823 from the American Heart Association.

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