Abundant defective viral particles budding from microglia in the course ofretroviral spongiform encephalopathy

A pathogenetic hallmark of retroviral neurodegeneration is the affinity of neurovirulent retroviruses for microglia cells, while degenerating neurons are excluded from retroviral infections. Microglia isolated ex vivo from ra ts peripherally infected with a neurovirulent retrovirus released abundant mature type C virions; however, infectivity associated with microglia was v ery low. In microglia, viral transcription was unaffected but envelope prot eins were insufficiently cleaved into mature viral proteins and were not de tected on time microglia cell surface. These microglia-specific defects in envelope protein translocation and processing not only may have prevented f ormation of infectious virus particles but also may have caused further cel lular defects in microglia with the consequence of indirect neuronal damage . It is conceivable that similar events play a role in neuro-AIDS.