Multiplication of lymphocytic choriomeningitis virus in thymocytes during its persistence in mice.
Persistence of lymphocytic choriomeningitis (LCM) virus in mice infected in utero or neonatally is due to impairment of the specific subsets of thymus-dependent lymphocytes which, in the adult normal mouse, are involved in elimination of LCM virus. Virus-thymocyte interactions were studied since it was likely that this impairment takes place in the thymus. Using an infectious centre assay, we found that about 1% of the thymocytes from foetal and neonatal mice were productively infected by the virus while thymocytes from older mice were refractory to infection. The infected cells were Thy 1-positive and agglutinated by peanut lectin together with immature lymphocytes. Later, when virus persistence was established, the number of infected thymocytes declined to about 0.1% and these cells were not agglutinated by lectin. The results are compatible with the assumption that thymic precursor T-cells capable of elimination LCM virus are chronically infected by the virus and rendered non-functional.
D000375:Aging; D000818:Animals; D002454:Cell Differentiation; D008216:Lymphocytic Choriomeningitis / Q000382:microbiology*; D008217:Lymphocytic choriomeningitis virus / Q000254:growth & development*; D051379:Mice; D013601:T-Lymphocytes / Q000382:microbiology*; D013997:Time Factors