THE interaction of lymphocytic choriomeningitis (LCM) virus with mouse tissues has been discussed recently1–5. The fulminating disease, which occurs in adult mice after intracerebral inoculation with LCM virus, can be ameliorated by several treatments known to impair the immune response of the host, such as X-rays6, amethopterin7, thymectomy8 and anti-lymphocyte serum9. The pathology of the disease10 supports the current view that an immune reaction by the host against the virus or a virus product, located in or on infected cells, plays an essential part in its pathogenesis. A similar mechanism may be important in the chronic autoimmune-like disease in virus carrier mice2,5. Further elucidation of this disease mechanism depends on understanding the nature of the immune response and its target. A question of considerable interest is what the consequences might be for virus infected cells in the event of an immune response against the virus or a virus product. Here we report preliminary experiments involving transplantation of cells from virus carrier mice to syngeneic non-infected recipients which suggest that tissues of mice chronically infected with LCM virus undergo an antigenic change which can be detected by transplant rejection.
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HOLTERMANN, O., MAJDE, J. Rejection of Skin Grafts from Mice chronically infected with Lymphocytic Choriomeningitis Virus by non-infected Syngeneic Recipients. Nature 223, 624 (1969). https://doi.org/10.1038/223624a0
MOUSE PARVOVIRUS INFECTION POTENTIATES ALLOGENEIC SKIN GRAFT REJECTION AND INDUCES SYNGENEIC GRAFT REJECTION1
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