The behavior of a fixed strain of Eastern equine encephalomyelitis virus was studied in guinea pigs after intraocular inoculation. Such inoculation concerns the central and not the peripheral nervous system.
The susceptibility to intraocular injection lies midway between the highly virulent intracerebral and the quite avirulent peripheral routes. The virus must act for 10 to 13 hours in order to induce a fatal infection. Removal of the inoculated eyeball before this interval almost always prevents fatality although it may allow immunity to develop. The virus, at suitable intervals after injection into the eye, may be recovered from successive and appropriate optic centers before it is demonstrable in non-optic portions. Approximately 24 hours are required for the virus to reach a significant concentration in the contralateral geniculate body, 36 hours in the contralateral visual cortex. Significant amounts of virus may be present in the optic chiasm and tract prior to involvement of the higher centers.
Virus placed in contact with the retina produces an insignificant, essentially non-specific reaction comparable to that produced at the site of direct intracerebral inoculation. In the retina there is no ganglion cell necrosis unless there is a complicating intraocular infection. In the cerebral visual centers the first reaction is inflammatory and interstitial, and may appear in the lateral geniculate body as early as 24 hours after injection. Neuronal necrosis is not the primary action of the virus on the nervous system in these experiments. The distribution of lesions in the brain is in excellent agreement with the method of direct testing for virus content, and is far more accurate than the latter.
The virus in its primary distribution through the nervous system follows the nerve pathways of the optic system. This occurs within the central nervous system, where presumably there is first an involvement of the nerve cell body and then a spread along the cell process or axone.