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lüll T cell memory specific for self and non-self antigens in rats persistently infected with Borna disease virus Rott O; Herzog S; Cash EClin Exp Immunol 1993[Sep]; 93 (3): 370-6We have studied CD4+ Th1 T cell responses in Borna disease (BD), a virus-mediated immune disease of the central nervous system (CNS), and demonstrate the priming of virus-specific as well as autoreactive T cells specific for myelin antigens in the course of viral infection. The fate of these in vivo generated T cells was subsequently assessed by in vitro proliferation assays with lymphocytes from different lymphoid organs of diseased animals over a long period of time. Virus-specific T cell responses continuously decreased during the establishment of persistent infection and could no longer be detected after 5-6 months post infectionem, when inflammatory reactions in the brain had ceased. By contrast, autoantigen-specific T cells kept their ability to mount characteristic secondary responses--although at an overall rather low level--over long periods of time; these autoreactive T cells homed to a specific lymphoid organ, the perithymic lymph node. Our study thus describes for the first time a complete decline of virus-specific T cell memory in a persistent viral infection, and raises the question how long-lasting T cell autoreactivity is controlled.|*Immunologic Memory[MESH]|Amino Acid Sequence[MESH]|Animals[MESH]|Borna Disease/*immunology[MESH]|Cross Reactions[MESH]|Female[MESH]|Molecular Sequence Data[MESH]|Myelin Basic Protein/immunology[MESH]|Myelin Proteins/immunology[MESH]|Myelin Proteolipid Protein[MESH]|Rats[MESH]|Rats, Inbred Lew[MESH]|T-Lymphocytes/*immunology[MESH] |