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Viral acute respiratory infections (ARIs) are associated with cluster of differentiation (CD)8+ T cells that exhibit diminished production of cytokines and cytotoxic molecules. Though these cells recognize major histocompatibility complex (MHC)-I–restricted viral epitopes, ex vivo stimulation of these cells with these same viral peptides fails to elicit production of interferon (IFN)γ, interleukin (IL)-2, or tumor necrosis factor (TNF)-α; degranulation as measured by CD107a staining; or other features of functional CD8+ T cells. This is a unique feature of viral ARI because T-cell dysfunction occurs in chronic rather than acute infections of many other organs. Although CD4+ regulatory T cells (Tregs) contribute to CD8+ T-cell dysfunction, recent work on a variety of viruses has identified inhibitory receptors as a key mediator of this phenotype. Programmed cell death 1 (PD-1) is the most well-studied inhibitory receptor in T-cell impairment, but there is growing evidence that other inhibitory receptors also play a role. The tendency of CD8+ T cells to have significantly reduced functionality in the context of respiratory virus infection has been termed "T cell impairment".

Reining in the CD8+ T cell: Respiratory virus infection and PD-1-mediated T-cell impairment