Viral infection states, immune control, and adult cognition: evidence across latency, persistence, and post-acute...

Viral infections can leave latent genomes, persistent reservoirs, or prolonged host responses after the presenting illness has resolved. This Review organizes their relevance to adult cognition around three overlapping infection-state prototypes: latency with episodic reactivation, chronic persistence, and acute infection with post-acute host responses. We examine how local antiviral surveillance, antigen-driven T-cell dysfunction, innate immune memory, and inflammatory resolution shape neurovascular and glial responses. Complement-mediated synaptic remodeling, proteostatic disruption, and immunometabolic changes provide additional mechanistic links. The synthesis distinguishes persistent cognitive symptoms, longitudinal cognitive trajectories, and clinical or biomarker-defined neurodegeneration. A dedicated vaccination section examines pathogen-specific protection, adjuvant biology, and heterologous immune effects, while antiviral studies address cognitive change during viral suppression or after clearance. These findings motivate event-triggered studies of reactivation, treatment-anchored studies of persistence, and acute-to-recovery studies of post-infectious cognition, complemented by targeted experimental perturbation. Linking infection state, immune function, and outcome-specific follow-up provides a practical route from broad epidemiological associations to testable mechanisms and modifiable biological processes.