The virus of avian encephalomyelitis is distinct from that of equine encephalomyelitis and is clearly a virus sui generis. The striking feature of its properties is its narrow range of host susceptibility—only the avian species are responsive to inoculation; ordinary laboratory animals are apparently resistant, even to large numbers of chicken cerebral infective doses. In addition, it is probable that its size is in the range of that of the equine virus. Studies also reveal that the virus is not easily sedimented by centrifugation (that is, at 5400 R.P.M. for one hour in the angle centrifuge and at 12,000 R.P.M. for one hour in the open air centrifuge) and is resistant to the action of glycerol and to drying. It is readily filtrable through Seitz one and two disc filters, through Berkefeld V and N candles, and is active in dilutions in broth up to 10^–6. It passes through gradocol membranes of 73 mµ average pore diameter at least (the end-point has not as yet been definitely determined).

An attack of the experimental disease leads to development of resistance to reinoculation and of antibodies in the serum. Old birds are reported as being refractory to infection, both in nature and in the laboratory (1, 2). Whether this resistance in mature animals is due to earlier exposure to infection, or to the development of structural or physiological barriers to invasion by the virus, remains still to be determined.

Under experimental conditions, the route by which the virus acts uniformly to induce disease is the intracerebral. Yet in certain instances other peripheral ways of inoculation such as the intraperitoneal, subcutaneous, intradermal, intravenous, intramuscular, intrasciatic, may also be effective. Thus far, in limited experiments, feeding, or instilling nasally, or injecting into the vitreous body the infective agent has been ineffective. Whether the viral progression is axonal from peripheral sites is still to be determined; as should be also the question whether it multiplies in any of the organs other than the central nervous tissues. The virus was not detected in the blood during the period of incubation or during the acute phases of the experimental disease. So that unless it is found that other animals harbor the virus, or that still other sources of it exist as yet not disclosed, it is not likely that the disease is disseminated by a blood-sucking insect. The actual portal of entry and the factor in the spread of the disease in nature is still obscure, since the evidence here presented is still too incomplete to elucidate these problems.

The pathological lesions induced are of interest. The neuronal reaction resembles that brought about by axonal disturbance (axon reaction, Nissl's or retrograde degeneration). The question may well be asked whether there may not be here an initial injury by the virus to the axonal process of the neuron, which in turn induces the retrograde changes in the cell body. This has as yet to be studied, as well as the possibility of viral progression along an axonal route with or without concurrent multiplication. The significance of the second major lesion in the central nervous system, namely, the generally marked perivascular reaction, is also still to be determined.

Finally, the only observable and histopathological change in organs other than the central nervous tissues (in which we have not as yet noted the change) is in the hyperplasia of the normally present lymphoid islands. One is impressed by the prodigious numbers of lymphoid elements surrounding the vessels of the central nervous system and the question here is whether these hyperplastic areas serve as depots to supply the cells for this perivascular reaction.