Protection of C58 mice from lactate dehydrogenase-elevating virus-induced motor neuron disease by non-neutralizing antiviral antibodies without interference with virus replication.

The paralytic poliomyelitis induced in old, immunosuppressed C58 mice by a primary infection with the lactate dehydrogenase-elevating virus (LDV) is prevented by the presence of anti-LDV antibodies in the virus inoculum or by passive transfer of LDV-free plasma from chronically LDV-infected mice one day before infection. Non-neutralizing antibodies were protective and specifically directed to the lowest molecular weight form of the envelope glycoprotein of LDV (VP-3), which seems to exist in virions in at least ten molecular forms ranging from 24 to 44 kDa. The antibodies did not prevent the productive infection of the subpopulation of macrophages that represents the primary permissive cell type in the mouse as evidenced by normal plasma LDV levels nor the spread of LDV to the central nervous system. Many non-neuronal cells containing LDV RNA were detected by in situ hybridization in the spinal cords of mice that had been infected with LDV in the presence of protective antibodies. However, no LDV RNA-positive neurons were detected, which are normally found coincidental with the development of paralytic symptoms in LDV-infected C58 mice. We propose that an early event after infection is critical for the infection of neurons and is inhibited by the presence of non-neutralizing antibodies to the LDV glycoprotein.