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From the Department of Pathology, Cornell University Medical College, New York, New York 10021, and the Department of Microbiology and Immunology, State University of New York, Downstate Medical Center, Brooklyn, New York 11203
Abstract
Coxsackie virus B3, inoculated i.p., replicated to high titer in the hearts of adult CD-1 and BALB/c mice but virus growth was completely suppressed 6 to 8 days after infection. On day 6 histologic examination showed that the hearts were infiltrated with mononuclear inflammatory cells which surrounded foci of necrotic myofibers. CD-1 animals survived the infection but most BALB/c mice died 8 to 14 days after virus challenge. CD-1 mice pretreated with rabbit anti-thymocyte serum (ATS) and T lymphocyte-deprived BALB/c mice (thymectomized, lethally irradiated, and bone marrow reconstituted) exhibited no reduction in their capacity to terminate viral replication suggesting that the development of effective anti-Coxsackie viral resistance occurred independently of T cell function. In addition, evidence was obtained implying that antiviral antibody synthesis during the 1st week of infection was not T cell dependent. However, observations in ATS-treated mice suggested that at later intervals T cells were required for optimal serum antibody production.
T cell dependent reactions were also found to play an important role in the pathogenesis of the heart disease induced by the virus. Thus administration of ATS greatly suppressed the production of inflammation and tissue injury in infected hearts of CD-1 mice. Similarly, T cell deprivation protected BALB/c mice against lethal infection. Moreover, the degree of cardiac inflammation and necrosis in virus-infected T cell-deprived BALB/c mice was significantly less than that found after infection of both intact mice and thymectomized irradiated mice which had been reconstituted with both bone marrow and thymus cells.
Footnotes
1 This work was supported in part by Grant-in-Aid 71-969 from the American and the Somerset County, New Jersey, Heart Associations and National Institutes of Health Grants AI 10080 and TO1-GM-00078.
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