Neurological complications of primary HHV6 infection, mainly HHV-6B, in childhood include seizures, hemiplegia, meningoencephalitis and residual encephalopathy of which outcomes remain uncertain [ 4 ]. Neuronophagia, microglial nodules and lympho-histiocytic, predominantly perivascular infiltrations are encountered in various regions of the brain. Cerebellum and basal ganglia are reported to be equally involved during EBV infection, next to cerebral hemisphere. Like most arbovirus infections, LACV infections are generally subclinical or present as a self-limiting febrile disease with headache, fever, nausea and vomiting with minimal neurological involvement. Rabies encephalitis in humans: The disease spectrum is similar to that of EV infections, although HPeV infection is almost exclusively seen in children. Infection by neurotropic viruses as well as the resulting immune response can irreversibly disrupt the complex structural and functional architecture of the central nervous system, frequently leaving the patient or affected animal with a poor or fatal prognosis.
Apart from mosquito-transmitted infection, CHIKV can be transmitted from viremic mother to child during birth.
Neurotropic virus infections as the cause of immediate and delayed neuropathology
RABV is prevalent throughout the world with only few countries being rabies free. The transport of the virus from its primary replication sites to the brain has not been fully elucidated, and may be realized by crossing the blood—brain barrier or via retrograde transaxonal transport . Besides immediate and direct effects, there are several neurological disorders often associated with autoimmune mechanisms that are assumed to be delayed virus-induced disorders: Lethal outcomes are associated with diffuse edema, brain hemorrhage, hepatocellular degeneration, alveolar hemorrhage and interstitial pneumonia [ 2762 ]. The HPeV species are only found in primates and now consists of 16 types [ 12 ].