neurovirulence

Neurovirulence is the capacity of a pathogen, toxin, or genetic construct to invade the nervous system and cause disease within neural tissue. It reflects several intersecting properties, including neurotropism (preference for neural cells), neuroinvasion (entry into the central nervous system), and neurotoxicity (direct damage or dysfunction of neural elements).

Neurovirulence is a key factor in the pathogenesis of various neurotropic pathogens, such as certain viruses and bacteria, and can contribute to encephalitis, meningitis, demyelination, or other neurological syndromes. Determinants of neurovirulence include pathogen genetic factors, host receptor usage, immune responses, and the integrity of barriers such as the blood–brain barrier. Host factors, including age, genetics, and prior immunity, also influence susceptibility and disease severity.

Assessment of neurovirulence often involves in vivo models to observe clinical and histopathological CNS outcomes, complemented by in vitro studies of neural cell infection, viral replication in neural tissue, and molecular analyses of virulence determinants. In public health and clinical settings, neurovirulence has particular relevance for live-attenuated vaccines and gene therapy vectors, where unintended CNS toxicity must be minimized. Historical and contemporary frameworks use neurovirulence testing to evaluate safety margins, with poliovirus neurovirulence serving as a well-known benchmark in vaccine development.

In research contexts, understanding neurovirulence informs risk assessment for emerging pathogens and guides strategies to reduce neural toxicity, such as attenuation, targeted delivery, or enhanced containment. The concept also intersects with neuroinvasion research in prions and other agents where CNS involvement determines clinical outcomes. Overall, neurovirulence describes the specific potential of a biological agent to affect the nervous system, shaping both disease understanding and safety practices.