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Respiratory viral infections remain a leading cause of morbidity and mortality. Using a murine model of human metapneumovirus (HMPV), we identified recruitment of a C1q-producing inflammatory monocyte population concomitant with viral clearance by adaptive immune cells. Genetic ablation of C1q led to reduced CD8 (+) T cell function. Production of C1q by a myeloid lineage was sufficient to enhance CD8 (+) T cell function. Activated and dividing CD8 (+) T cells expressed a putative C1q receptor, gC1qR. Perturbation of gC1qR signaling led to altered CD8 (+) T cell IFN-γ production and metabolic capacity. Autopsy specimens from fatal respiratory viral infections in children demonstrated diffuse production of C1q by an interstitial population. Humans with severe COVID-19 infection also demonstrated upregulation of gC1qR on activated and rapidly dividing CD8 (+) T cells. Collectively, these studies implicate C1q production from monocytes as a critical regulator of CD8 (+) T cell function following respiratory viral infection.