Type I interferon (IFN-I) promotes antiviral CD8⁺T cell responses, but the contribution of different IFN-I sources and signaling pathways are ill defined. While plasmacytoid dendritic cells (pDCs) produce IFN-I upon TLR stimulation, IFN-I is induced in most cells by helicases like MDA5. Using acute and chronic lymphocytic choriomeningitis virus (LCMV) infection models, we determined that pDCs transiently produce IFN-I that minimally impacts CD8⁺T cell responses and viral persistence. Rather, MDA5 is the key sensor that induces IFN-I required for CD8⁺T cell responses. In the absence of MDA5, CD8⁺T cell responses to acute infection rely on CD4⁺T cell help, and loss of both CD4⁺T cells and MDA5 results in CD8⁺T cell exhaustion and persistent infection. Chronic LCMV infection rapidly attenuates IFN-I responses, but early administration of exogenous IFN-I rescues CD8⁺T cells, promoting viral clearance. Thus, effective antiviral CD8⁺T cell responses depend on the timing and magnitude of IFN-I production.