Poliovirus is a neurotropic virus that selectively infects human motoneurons in vivo. The basis for the specificity of this infection is not fully understood. It has been suggested that this tropism occurs because motoneurons are the only neurons to express poliovirus receptors. We have examined this hypothesis by measuring the binding of 125I-labeled poliovirus type 1 to neural tissues. With this assay we have detected highly specific binding sites in human but not rodent neural tissue. Regional assays of binding in human central nervous system homogenates demonstrate that binding sites are not confined to motoneurons. Rather, they are widely distributed throughout the human neuraxis. Particularly in the forebrain, binding is more abundant in gray than white matter. For this reason, we performed tissue fractionation studies which indicate that poliovirus binding sites are enriched in synaptosomes, the subfraction of central nervous system gray matter tissue rich in synaptic endings. The preferential expression of poliovirus binding sites in synaptic endings may be an important factor in the motor tropism of this virus, inasmuch as the major category of neurons with synaptic endings outside the central nervous system are motoneurons; thus, particles of virus may preferentially bind to this cell type during poliovirus viremia.
Sera from 12 patients with amyotrophic lateral sclerosis (ALS) and 18 controls were screened for antineural antibodies using immunoblotting. No consistent differences were detected between ALS patients and controls, although antibodies to 52,000- and 70,000-dalton proteins in mouse spinal cord were somewhat more common in ALS sera. Antibodies to a protein of approximately 150,000 to 200,000 daltons were also evident. The 70,000- and 52,000-dalton proteins were detected in brain, cerebellum, and liver as well as spinal cord. Immunohistochemistry suggested antibody activity was directed at least in part to neurofilaments. While the antibodies to the 52,000- and 70,000-dalton proteins were more common in ALS than control sera (p less than 0.02 and less than 0.05, respectively), it is not clear from this initial study that this difference is of clinical or etiologic significance.
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