Abstract
Rabies virus is usually transmitted by an animal bite and the virus remains close to the site of the bite for a period of weeks during the incubation period. Subsequently, the virus spreads in peripheral or cranial nerves by retrograde fast axonal transport, and then spreads extensively in the central nervous system (CNS) by the same mechanism along neuroanatomical connections. The infection produces mild inflammatory changes in the CNS, but degenerative neuronal changes are not prominent. Rabies virus later spreads centrifugally to multiple organs along sensory and autonomic nerve pathways to salivary glands (in rabies vectors), skin (basis of skin biopsy as a diagnostic test), heart, gastrointestinal tract, adrenals, and other organs. Degeneration of neuronal processes has recently been recognized, which is related to oxidative stress. The blood-brain barrier plays a role in excluding immune effector cells from entering the CNS in street rabies virus infection. There is usually a fatal outcome in rabies in humans and animals.
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