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

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.