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  • Title: Temperature-sensitive mutant of coxsackievirus B3 establishes resistance in neonatal mice that protects them during adolescence against coxsackievirus B3-induced myocarditis.
    Author: Gauntt CJ, Paque RE, Trousdale MD, Gudvangen RJ, Barr DT, Lipotich GJ, Nealon TJ, Duffey PS.
    Journal: Infect Immun; 1983 Feb; 39(2):851-64. PubMed ID: 6299950.
    Abstract:
    Inoculation of neonatal CD-1 mice by multiple routes with an amyocarditic temperature-sensitive (ts) mutant (ts 1) derived from a myocarditic parent variant of coxsackievirus B3 (CVB3(m)) resulted in approximately half of the neonates surviving to adolescence. Challenge of the ts 1 survivors with CVB3(m) did not induce myocarditis, as assessed by histological examination of heart tissues. Virus was not detected in heart tissues of adolescent ts 1 survivors, but inoculation of these mice with CVB3(m) resulted in virus concentrations similar in titers to those found in CVB3(m)-inoculated normal adolescent mice. The ts 1 survivors did not contain detectable levels of anti-CVB3(m) neutralizing antibody, but upon challenge with CVB3(m) they produced antibody more rapidly and to higher titers than did normal CD-1 adolescents after primary inoculation with CVB3(m). Cell-mediated immunity in ts 1 survivors was compared with that of normal mice after challenge with CVB3(m). The capacity for production of migration inhibitory factor was assessed by the agarose droplet cell migration inhibition assay, using peritoneal exudate cells and a CVB3(m) cell lysate or KCl-extracted antigens from heart tissues of CVB3(m)-inoculated mice. Migration inhibitory factor activity was not detected in cultures of splenic leukocytes from ts 1 survivors of CVB3(m)-inoculated ts 1 survivors, but it was readily detected in cultures of splenic leukocytes from CVB3(m)-inoculated normal adolescent mice. The [(3)H]thymidine stimulation assay, performed with splenic lymphoid cells and purified CVB3(m) particles, revealed that lymphocytes from normal mice, whether inoculated with CVB3(m) or not, were not stimulated by CVB3(m) particle antigens, whereas lymphoid cells from a significantly higher proportion of ts 1 survivors, whether inoculated with CVB3(m) or not, responded with a stimulation index >/=2.0. The cells responding with positive stimulation were T lymphocytes. A higher proportion of normal mice and ts 1 survivors, both inoculated with CVB3(m), contained splenic cytotoxic T lymphocytes with higher reactivity against CVB3(m)-infected neonatal skin fibroblasts than against normal skin fibroblasts, as assessed by a (51)Cr release assay. The group of uninoculated ts 1 survivors present as a high proportion of individuals with cytotoxic T-lymphocyte reactivity against both uninoculated and CVB3(m)-inoculated skin fibroblasts. However, ts 1 survivors and normal mice possessed the same proportions of splenic lymphocytes carrying either allele for Lyt 1 and Lyt 2 surface markers. The results suggest two mechanisms by which ts 1 survivors exhibit resistance to CVB3(m) induction of myocarditis, namely, the rapid production of high-titered anti-CVB3(m) neutralizing antibody in response to CVB3(m) inoculation and altered cell-mediated immune responses against CVB3(m)-induced viral or novel cellular antigens. The data are compatible with the notion that an immune deviation mechanism, thought to be controlled through a mechanism requiring suppressor cell activity which inhibits macrophage activation in ts 1 survivors, protects these mice from induction of myocarditis.
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