Characteristics of the persistence of the tick-borne encephalitis virus against a background of experimentally induced allergic encephalomyelitis in M. rhesus monkeys

• Published in: Voprosy virusologiĭ Vol. 27; no. 4; p. 409
• Main Authors: Pogodina, V V, Ravkina, L I, Malenko, G V, Fokina, G I, Bochkova, N G
• Format: Journal Article
• Language: Russian
• Published: Russia (Federation) 01-07-1982
• Subjects: Animals; Antibodies, Viral - analysis; Antibody Formation; Chronic Disease; Encephalitis Viruses, Tick-Borne - isolation & purification; Encephalitis Viruses, Tick-Borne - pathogenicity; Encephalomyelitis, Autoimmune, Experimental - immunology; Encephalomyelitis, Autoimmune, Experimental - microbiology; Encephalomyelitis, Autoimmune, Experimental - pathology; Macaca mulatta
• ISSN: 0507-4088

Asymptomatic persistence of tick-borne encephalitis (TBE) virus was modeled by subcutaneous inoculation; the virus and the antigen were detected up to 307 days by the cell co-cultivation, tissue explants, and immunofluorescence methods. At early and late periods of the persistent infection (1 1/2, 8 1/2, or 10 1/2 months) for the purpose of its stimulation, an autoimmune disease, experimental allergic encephalomyelitis (EAE), running a course of the type of delayed hyperergic reaction was induced in the animals by inoculation of an encephalitogenic mixture (EM). After EM inoculation, a chronic demyelinating process developed in the CNS without the involvement of neurons; proliferation of immunocompetent cell elements was observed in the spleen and lymph nodes; a short-time or stable stimulation of TBE-specific humoral immunity was observed. Against the background of the development of chronic EAE and a short-time stimulation of humoral immunity, persistence of TBE virus was prolonged for over 2 years, its location being unchanged (different parts of the brain, spleen). Despite long-term persistence of TBE virus in the CNS, no clinical and morphological symptoms of chronic TBE were found. Possible mechanisms of the effect of this stimulating factor favouring the activation of the persisting TBE virus on the one hand and limiting this process on the other are discussed.