Figure 3
Figure 3. Systemic replication of LCMV is inhibited by IFN-I produced by hematopoietic cells. (A) WT mice, irf7−/− mice, and BM chimeras (WT-BM > WT, WT-BM > irf7−/−, irf7−/−-BM > WT and irf7−/−-BM > irf7−/−) were infected with 200 PFU LCMV. After 4 days, viral titers were analyzed (n = 4-5). (B) WT mice, WT mice depleted of CD8+ T cells and NK cells, and Rag−/− mice depleted of NK cells were infected with 200 PFU LCMV-WE intravenously. Virus titers were analyzed in spleen liver, lung, and kidney 3 days after infection. (C) MC57 cells were treated with different concentrations of IFN-α and then infected with VSV or LCMV (MOI 0.001). After 6, 12, and 24 hours, infectious virus was analyzed in the supernatant.

Systemic replication of LCMV is inhibited by IFN-I produced by hematopoietic cells. (A) WT mice, irf7−/− mice, and BM chimeras (WT-BM > WT, WT-BM > irf7−/−, irf7−/−-BM > WT and irf7−/−-BM > irf7−/−) were infected with 200 PFU LCMV. After 4 days, viral titers were analyzed (n = 4-5). (B) WT mice, WT mice depleted of CD8+ T cells and NK cells, and Rag−/− mice depleted of NK cells were infected with 200 PFU LCMV-WE intravenously. Virus titers were analyzed in spleen liver, lung, and kidney 3 days after infection. (C) MC57 cells were treated with different concentrations of IFN-α and then infected with VSV or LCMV (MOI 0.001). After 6, 12, and 24 hours, infectious virus was analyzed in the supernatant.

Close Modal

or Create an Account

Close Modal
Close Modal