T cell memory specific for self and non‐self antigens in rats persistently infected with Borna disease virus

• Published in: Clinical and experimental immunology Vol. 93; no. 3; pp. 370 - 376
• Main Authors: ROTT, O., HERZOG, S., CASH, E.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.09.1993; Blackwell
• Subjects: Amino Acid Sequence; Animals; autoreactivity; Biological and medical sciences; Borna Disease - immunology; Borna disease virus; Cross Reactions; Experimental viral diseases and models; Female; Immunologic Memory; Infectious diseases; Medical sciences; Molecular Sequence Data; Myelin Basic Protein - immunology; Myelin Proteins - immunology; Myelin Proteolipid Protein; Rats; Rats, Inbred Lew; T cell homing; T cell memory; T-Lymphocytes - immunology; Viral diseases; viral persistence; Immunological memory; Immune response; Rat; Borna virus; Rodentia; Central nervous system; Helper cell; Cellular immunity; Infection; Virus; Vertebrata; Mammalia; Autoantigen; Animal; Persistent infection; Viral disease; T-Lymphocyte; Borna disease; Brain (vertebrata)
• ISSN: 0009-9104; 1365-2249
• DOI: 10.1111/j.1365-2249.1993.tb08187.x

SUMMARY We have studied CD4+ Thl 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 autoreacti ve 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 aulorcaclivily is controlled.