Host Factors Regulating Viral Clearance

Role of natural killer cells in experimental murine myocarditis

“…In an attempt to further delineate roles played by these two nonspecific defense systems on CVB3-induced myocarditis, mice were administered reagents to deplete NK cells or IFN, or were given IFN ( Table 3). Administration of either IFN-7 or -/3 significantly reduced myocarditic lesion number without effecting NK cell activity as previously reported [12,24]. Studies with IFN-7 showed that 2.5 x 105 units were required to achieve a reproducible anti-myocarditis effect whereas 2.5 x 104 units of IFN-/3 Mice were inoculated by intraperitoneal route with 105 pfu on day 0.…”

“…and remains elevated for another 2 days. Virus induction of NK cell activity follows significant increases in virus titers in blood [12] and parallels an increase in IFN levels in serum [13]. The dosage of virus is not critical to induction of NK cell activity, as intraperitoneal inoculation of doses between 102 and 108 plaque-forming units (pfu) of virus induced similar levels of activity, although a dose of 105 pfu generally induced maximum activity [13].…”

Benign human enterovirus becomes virulent in selenium‐deficient mice

“…Because the immune system of CVB3-infected mice may both aid in viral clearance as well as contribute to heart pathology [Chow et al, 1992;Gauntt et al, 1988;Van Houten and Huber, 19891, and because Se deficiency has been reported to adversely affect a number of immune functions [Combs and Combs, 19861, we tested serum for the presence of neutralizing antibodies against coxsackievirus B3, the production of which requires both T and B cell activity. Both Se-deficient and Se-adequate CVB310-inoculated mice developed equivalent neutralizing antibody titers against CVB3 virus (ranging from 1/30 to 111601, suggesting that Se deficiency did not induce a generalized immune dysfunction.…”

Differential Behaviour in Pancreas and Heart of Two Coxsackievirus B3 Variants

“…The in ability to multiply in myocardial tissues has been attributed by Gauntt et al [32] to a rapid clearance not operative for other intratypic variants or to a lack of initial replication in cells readily permissive to other myocarditic viral strains.…”