Replication of Langat virus in immunocompetent cells of mice subjected to immobilization stress.

Immobilization stress (hypokinesis) in Balb/c mice may aggravate asymptomatic infection with Langat virus (strain TP-21) as evidenced by 4-fold increased lethality in comparison with control animals. The virus levels in the spleen and brain of stressed and infected mice and the in vitro yield of the virus in immunocompetent cells derived from stressed mice were significantly higher than in controls. Enhanced virus replication in latter cells may contribute to increased accumulation of the infectious agent in lymphatic tissues, which would facilitate virus invasion into CNS followed with acute disease and death of animals.

H-2 restricted regulation by soluble autoantigens of the tick-borne encephalitis virus-induced autoreactive T-effector and T-suppressor lymphocytes in mice.

Soluble autoantigens (mouse red blood cells lysed by sonication) blocked in vitro the antigen-recognizing receptors of tick-borne encephalitis (TBE) virus-induced autoreactive T-lymphocytes (ARTL), effectors of the local graft-versus-host reaction (GVHR) in a syngeneic system and prevented the development of GVHR in vivo. Antigen-recognizing receptors were also found on T-suppressors (Ts) that became activated during experimental tick-borne encephalitis in mice and inhibited the activity of ARTL. The interaction between these receptors and autoantigens in vitro resulted in a loss of the ability of Ts to inhibit in vivo the ARTL-mediated GVHR.

Variability of Powassan virus cultured in tissue explants and organism of Hyalomma anatolicum ticks.

The variability of Powassan virus was studied during successive passages in Hyalomma anatolicum ticks or prolonged reproduction in their tissue explants. It had been shown that in the course of tick passages and during reproduction in the explants, pathogenicity of the virus in respect to causing acute disease in mice after peripheral inoculation was decreased, while virus ability to cause death after intracerebral (i.c.

Role of macrophages in the pathogenesis of experimental tick-borne encephalitis in mice.

In vivo phagocytosis activity of macrophages (PAM) was temporarily suppressed in mice by application of a suspension of microscopic from particles. As demonstrated, a reversible block of 70% of PAM was accompanied by a marked increase of the lethality during the acute tick-borne encephalitis (TBE) virus infection. Asymptomatic persistence of TBE virus in the brain was 4 times more frequent in mice with PAM defect than in immuno-competent mice.