Abstract
The evidence increases that circulating antibodies play a minor part in the resistance to poliomyelitis both in man and in monkeys. Antisera have commonly failed to prevent the disease even when used in large quantities or to modify its course when used thera-peutically; the disease has developed both in monkeys and in man even though they possessed neutralizing blood of high titer; antibodies have been found in 75 to 85% of normal adults regardless of previous poliomyelitis; neither resistance nor susceptibility to the disease in man or monkey presents any close correlation to the presence or absence of demonstrable antibodies. In consequence of these findings, some authors have attempted to seek an answer to the problem of immunity in this disease on an hormonal basis, with conflicting results, others have raised the query of nutritional deficiencies, while still others have employed the term “tissue immunity” to indicate the resistance, due to obscure factors, apparently independent of humoral antibodies. In attempting to unravel the varying reports on this type of resistance, one must bear in mind the primary cellular basis of immunity and anaphylaxis, the many instances of interference phenomena sometimes entirely non-specific, as well as the possibility of closely bound antibodies such as those demonstrated with the Shope rabbit papilloma virus. Recently Howe and Bodian have summarized their extensive investigations on neural mechanisms in poliomyelitis in a telling monograph. Closely related to the problem of our paper is their demonstration that a second attack of poliomyelitis can be induced in rhesus monkeys either with homologous or heterologous strains of virus provided a different portal of entry is employed, thus bringing the virus in contact with nervous tissue not previously involved with the virus.
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