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STUDIES ON PSEUDORABIES (INFECTIOUS BULBAR PARALYSIS, MAD ITCH : III. THE DISEASE IN THE RHESUS MONKEY, MACACA
1Department of Animal and Plant Pathology of The Rockefeller Institute for Medical Research, Princeton, N. J., and the Bacteriological Department, Lister Institute of Preventive Medicine, London.
Abstract:
In the monkey (M. mulatto) the virus of pseudorabies, pantropic in the rabbit, behaves as a strict neurotrope. Infection, usually fatal, readily follows intracerebral and intracisternal inoculation of rabbit virus, and often intrasciatic inoculation; the symptomatology of the ensuing disease is described. In a limited number of experiments no infection resulted from intradermal, intramuscular or intravenous inoculation. Nerve and glial cells are primarily attacked by the virus, but no cytological or other evidence of susceptibility of non-nervous tissue or of growth of virus outside the nervous system was obtained. Certain cortical areas, of which the principal are the pyriform area, cornu Ammonis, island of Reil, lower lip of the Sylvian fissure and basal surface of the frontal lobe, are affected far more severely than are other parts of the nervous axis; the reasons for this elective distribution of the most severe lesions, seen alike after intracerebral and intrasciatic inoculation and analogous perhaps to that in poliomyelitis and louping-ill, are not obvious. Other areas of the nervous system are relatively insusceptible to the action of the virus. Cases showing clinically only a febrile reaction without definite nervous symptoms may later exhibit marked residual lesions at the sites of election. The blood and cerebrospinal fluid play no apparent rôle in disseminating the virus, which, after intrasciatic inoculation, spreads upwards by the nervous path. Some suggestion was received from the experiments that in monkeys possessed of immunity to B virus (Sabin and Wright, 1934) pseudorabic infection is less likely to prove fatal than in animals not so immune, but the observations made were insufficiently numerous to be of statistical value. The sera of 6 out of 26 monkeys were found to contain antibodies neutralising B virus; these 6 monkeys were all included in one batch of 7 received at one time from the dealer.
Insights
Pseudorabies virus in rhesus monkeys (M. mulatto) acts as a neurotrope, primarily infecting nerve and glial cells. Fatal infections occur via direct brain or sciatic nerve inoculation, with specific cortical areas showing severe lesions.
Area of Science:
- Neurovirology
- Infectious Diseases
- Primate Models
Background:
- Pseudorabies virus (PRV), typically pantropic in rabbits, exhibits distinct behavior in non-rodent species.
- Understanding PRV neurotropism is crucial for disease management and vaccine development.
Purpose of the Study:
- To investigate the neurotropic potential and pathological effects of pseudorabies virus in rhesus monkeys (M. mulatto).
- To identify specific neural targets and pathways affected by PRV infection in primates.
Main Methods:
- Intracerebral, intracisternal, intrasciatic, intradermal, intramuscular, and intravenous inoculation of PRV in M. mulatto.
- Clinical observation, symptomatology documentation, and neuropathological examination of infected monkeys.
Main Results:
- PRV demonstrated strict neurotropism in M. mulatto, with intracerebral and intrasciatic routes leading to fatal infections.
- Primary viral attack targeted nerve and glial cells, with no evidence of extraneural replication.
- Specific cortical areas (e.g., pyriform cortex, hippocampus) exhibited severe, elective lesions, while other neural regions were less susceptible.
- Spread of the virus occurred along nervous pathways, particularly upwards from intrasciatic inoculation sites.
Conclusions:
- Pseudorabies virus functions as a strict neurotrope in rhesus monkeys, causing severe, often fatal, neurological disease.
- The virus exhibits elective distribution of lesions within the central nervous system, suggesting specific neuronal susceptibilities.
- Further research is needed to elucidate the mechanisms behind this elective neuropathology and potential host immune interactions.
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