The concept of neurotropism and selective vulnerability ("pathoclisis") in virus infections of the nervous system--a historical overview.

Abstract

Nervous diseases that we regard now to be of viral origin were known and described already in antiquity and in medieval times. Rabies, poliomyelitis and yellow fever belong to this category. The contagious nature of these diseases was suspected for centuries, and their symptomatology suggested that the brain is preferentially targeted by these infections. Not long after the advent of virology, the viral etiology of these diseases was proven. That such agents may have a special affinity to neural structures was first documented by experimental studies on rabies. Cantani (1888), Professor of Internal Medicine in Naples, laid down the concept of the neural spread of rabies: transection of limb nerves after peripheral inocu­lation prevented the evolution of the disease. One year later, two of his pupils, Di Vestea and Zagari (1889), published a more elaborate study on this subject in the Annales de l’Institut Pasteur; the recognition of the neural spread of rabies is attributed to these researchers in the literature. Schaffer (1890), in Budapest, provided evidence for the neural spread of rabies in humans based on histological studies: the most severe changes developed in spinal cord segments corresponding to the site of the animal bite. These early studies clearly established that the agent of rabies has such an elementary affinity to neural structures that it spreads exclusively along these pathways to the central nervous system (CNS).