Additionally, viral recrudescence was undetectable as late as 23 days p.i. Thus, we contend that–contrary to current thinking–T1IFN signaling is not required for the secondary response to viral infection, neither regulating the attrition, expansion, and secondary memory formation of memory CD8+ and CD4+ T cells, nor being required for establishing an antiviral state within host parenchymal cells. The gene discussed is CD8A; the disease is viral infectious disease.