title: Suppression of cell-mediated immunity by street rabies virus infection.
abstract: An attempt to define a severe suppression of cell-mediated immunity by street rabies virus infection was undertaken by using the mice lethally and peripherally infected with a street rabies virus (1088 strain). The cell-mediated cytotoxic (CMC) activity of the spleen cells from those mice once slightly increased until day 4 after infection but declined rapidly thereafter until their death on days 10 to 12 after infection. In parallel with a decrease of CMC response of the spleen cells from 1088-infected mice, proliferative response to Con A, IL-2 activity in the culture supernatants of Con A-induced proliferation, responsiveness to exogenously added IL-2 and to Con A to express IL-2R, of those cells became suppressed, and the marked decrease of the total number of spleen cells was observed. Selective depletion of CD4+ and CD8+ cells in the spleens, abnormalities of IL-1 and E-type prostaglandins (PGE2) production or production of inhibitory component able to block IL-2 activity by spleen cells were not observed and these factors did not appear to be associated with the suppression of proliferative response to Con A. However, an apparent association of CD8+ cells in the suppression of differentiation of pre-cytotoxic lymphocytes (CTL) into CTL was demonstrated in the co-culture experiments of the spleen cells from 1088-infected mice with spleen cells of mice infected with an attenuated rabies virus (ERA strain) which can induce higher levels of CMC response. There was no evidence of the productive replication of rabies virus in thymus and spleen of 1088-infected mice. The relationship of these observations to current theories on virus-induced immunosuppression was discussed.
authors.affiliation: Department of Microbiology, Oita Medical University, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Hirai
authors.forename: H
authors.initials: H
authors.lastname: Kawano
authors.forename: K
authors.initials: K
authors.lastname: Mifune
authors.forename: H
authors.initials: H
authors.lastname: Fujii
authors.forename: A
authors.initials: A
authors.lastname: Nishizono
authors.forename: A
authors.initials: A
authors.lastname: Shichijo
authors.forename: K
authors.initials: K
authors.lastname: Mannen
mesh_terms: D000818:Animals; D016516:CD4-CD8 Ratio; D002460:Cell Line; D002478:Cells, Cultured; D003208:Concanavalin A / Q000494:pharmacology; D007108:Immune Tolerance; D007375:Interleukin-1 / Q000096:biosynthesis; D007376:Interleukin-2 / Q000096:biosynthesis / Q000494:pharmacology; D008213:Lymphocyte Activation; D051379:Mice; D008805:Mice, Inbred A; D011818:Rabies / Q000276:immunology*; D011820:Rabies virus / Q000276:immunology / Q000502:physiology; D015375:Receptors, Interleukin-2 / Q000032:analysis; D013154:Spleen / Q000276:immunology* / Q000382:microbiology; D013601:T-Lymphocytes / Q000276:immunology; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology; D013950:Thymus Gland / Q000382:microbiology; D014407:Tumor Cells, Cultured
chemical_list: D007375:Interleukin-1; D007376:Interleukin-2; D015375:Receptors, Interleukin-2; D003208:Concanavalin A