Abstract
Once an animal has been infected in utero or neonatally with LCM virus, that virus can persist in most tissues throughout the animal’s life (11,29,30). This finding along with the inability to find free circulating antibody to LCM virus in such mice led Burnet to postulate in the late 1940’s that mice infected with LCM virus were immunologically tolerant to this agent (3). Doubts about the validity of this concept were first raised in the late 1960’s in our laboratory (16). While observing immunopathological and virological events in chronically infected mice, we found host immunoglobulin G (IgG), complement (C3, 3rd complement component) and LCM viral antigen(s) deposited in the renal glomeruli in a granular pattern (16). This picture of antigen, IgG and C3 deposits had been seen many times before in different diseases and is pathognomonic of immune complex deposits (5,6). This suggested that these mice, in spite of carrying persistent titers of LCM virus, were also mounting an anti-viral antibody response, the antibody complexing with virus in the circulation to form virus-anti-viral antibody (V-Ab) complexes which subsequently became trapped in the renal glomeruli. Later experimental work indeed showed both the presence of circulating V-Ab complexes (17,18) and of specific antibody to LCM virus (16,17,18). Later observations indicated that in some strains, i.e., NZB,(NZB x W)F1, about 15 to 20% of infected mice made detectable free circulating antibody by 6 to 9 months of age.
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Oldstone, M.B.A. (1973). Thymus-Dependent (T) Cell Competence in Chronic LCM Virus Infection. In: Lehmann-Grube, F. (eds) Lymphocytic Choriomeningitis Virus and Other Arenaviruses. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-65681-1_17
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DOI: https://doi.org/10.1007/978-3-642-65681-1_17
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