Viral Diseases of the Central Nervous System

Most meningitis and almost all encephalitis is of viral etiology (Table 36-3). Infections of the CNS arise, in the main, as a rare complication of a primary infection established elsewhere in the body which fortuitously spreads to the brain, usually via the bloodstream. Sometimes they occur following reactivation of a latent herpesvirus or papovavirus infection, particularly following immunosuppression. Overwhelming disseminated infections acquired peri-natally may also involve the brain.

Certain viruses have a predilection for particular parts of the CNS, and the clinical signs of the resulting disease often reflect this. For example, most enteroviruses do not go beyond the meninges, but polioviruses invade the anterior horn of the spinal cord and the motor cortex of the cerebrum, whereas rabies singles out Ammon's horn, herpes simplex virus the temporal lobes, and so on. Some viruses lyse neurons directly, and there is abundant evidence of inflammation in the brain (Fig. 36-4A); others do their damage in more subtle ways, leading to demyelination of nerves (Fig. 36-4B), sometimes involving immunopathologic processes.

One must distinguish between neurovirulence, that is, the ability to cause neurologic disease, and neuroinvasiveness, that is, the ability to enter the nervous system. Mumps virus, for example, displays high neuroinvasiveness, in that evidence of very mild meningitis accompanied by changes in the cerebrospinal fluid (CSF) are detectable in about half of all infections, but low neurovirulence, in that it rarely causes much damage. In contrast, herpes simplex virus (HSV) displays low neuroinvasiveness, in that it rarely invades the CNS, but high neurovirulence, in that when it does it often causes deva stating damage. Thus, neurotropism, the ability to infect neural ceils, is the product of neuroinvasiveness and neurovirulence. Moreover, not all neurotropic viruses are neuronotropic, that is, able to infect neurons, as are rabies virus, polioviruses, togaviruses, flaviviruses, and bunyaviruses; some viruses, such as the polyomavirus JC, preferentially replicate in nonneuronal cells like oligodendrocytes, causing demyehnation. Destruction of neurons has the most serious consequences as lost neurons are not replaced.

The blood-brain barrier, which tends to exclude viruses from the CNS, also limits access of lymphoid cells, antibodies, complement, etc.; only when inflammation disrupts the blood-brain barrier does the immune response come into play. Thus the barriers that inhibit virus invasion also deter virus clearance, accounting for the high frequency with which persistent virus infections involve the CNS.

The many and varied neurologic syndromes caused by viruses include meningitis, encephalitis, paralytic poliomyelitis, myelitis, polyneuritis, and several unusual demyelinating and degenerative syndromes.

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