POSSIBLE RETROVIRAL ORIGIN OF PRION DISEASES

The proposed hypothesis that a retrovirus might be involved in the eti ology of spongiform encephalopathies, integrates experimental results obtained from different fields of research. While retroviral genes the mselves may be responsible for neuronal death, a retrovirus may also c ause mutations in cellular genes. Hence, the prion gene may be altered by a retrovirus in the same way as a cellular proto-oncogene is alter ed to give an oncogene, either by transduction or by integration of th e provirus in its vicinity. In both cases, the resulting abnormal prio n protein, acting as a catalyst, may induce the formation of amyloid p laques. In addition, a wild type retrovirus may recombine to the vesic ular stomatitis virus (VSV) to give rise to a pseudotyped retrovirus c arrying the VSV G gene, known to induce spongiosis. Therefore a retrov iral etiology might explain why amyloid plaque and/or spongiosis are o r are not associated with neuronal death in prion diseases.