Why the study?
Does infection with virulent versus attenuated poliovirus type 1 cause different neural lesions in monkeys?
Does infection with virulent versus attenuated poliovirus type 1 cause different neural lesions in monkeys?
The study demonstrates that motor neuron death in poliovirus infection is due to direct viral replication and highlights histopathological differences between virulent and attenuated strains.
Direct replication drives motor neuron loss in primate polio models; leaves open human translation and vaccine attenuation mechanisms.
Using in situ hybridization techniques for viral RNA and employing a specific riboprobe, we have detected virus in neural cells of monkeys infected with poliovirus type 1 (PV-1) by the intraspinal route. In monkeys paralysed after inoculation of a neurovirulent revertant of PV-1/Sabin strain, viral RNA was detected in motor neurons and their processes, and in polymorphonuclear and small neural cells. Quantitative in situ hybridization provided evidence of viral replication in individual cells suggesting that the death of motor neurons was due to the direct effect of poliovirus replication in these cells. The histological study of neural lesions of monkeys paralysed after infection with the attenuated Sabin strain of PV-1 revealed two major differences compared to monkeys infected with a virulent strain: (i) the number of destroyed motor neurons was reduced and limited to the site of inoculation and (ii) the inflammatory reaction was localized but more intense. An account is given of the difference in histopathology induced by virulent and attenuated strains of PV-1 in the central nervous system.
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Couderc et al. (1989) studied this question.
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