Review evaluates mechanisms of Rift Valley fever virus neuroinvasion and antiviral drug strategies, highlighting the need for brain-penetrant therapeutics against delayed encephalitis.
Key Points
To examine the mechanisms underlying Rift Valley fever virus (RVFV) neuroinvasion and identify critical pharmacological requirements for developing antivirals that treat both systemic and central nervous system disease.
Reviewed published literature on RVFV entry pathways, blood–brain barrier disruption, neuroinflammatory cascades, and neuronal injury.
Evaluated antiviral drug candidates based on mechanism of action, timing of administration, tissue exposure, and efficacy within central nervous system models.
RVFV infection transitions from acute viremia and liver pathology to delayed encephalitis via route-dependent entry, neuroinflammation, and breakdown of the blood–brain barrier.
Existing antiviral development pipelines focus primarily on acute survival and liver viral clearance, demonstrating an urgent need to incorporate endpoints measuring brain pharmacokinetics, blood–brain barrier penetration, and delayed-treatment neuroprotection.