Two cases of necrotizing myelopathy were autopsied; one was complicated with lung carcinoma and the other with chronic type adult T cell leukemia (ATL leukemia). To our knowledge, they were the first cases of their type in Japan. In both cases, necrosis of the spinal cord was observed in the gray and white matter along most of its extent. Marked changes were found in the lumbar segment. The patients were not treated with intravenous cancer chemotherapy or irradiation. Immunohistochemical and electron microscopic examination revealed an extremely strong infection of herpes simplex virus (HSV) type 2. However, HSV type 1 and cytomegalovirus antigens were not detected.
A case of rapidly progressing ascending myelitis was necropsied. Necrosis was present throughout the whole length of the spinal cord and involved both the grey and white matter randomly. The perivascular lymphocytic infiltration in the spinal cord in the present case was more pronounced than that in the previously reported two cases of necrotizing myelopathy associated with malignancy. Using immunoperoxidase staining the presence of herpes simplex virus type 2 (HSV 2) antigen was demonstrated. Electron microscopic examinations revealed large numbers of HSV particles in the spinal cord. HSV 2 may be a common aetiological agent of necrotizing myelopathy and myelitis in Okinawa, an HSV 2 endemic area. In the present case, the necrosis was mainly found in the spinal cord but was also observed, to a very limited extent, in the brain.
Transient expression assays have shown that the varicella-zoster virus (VZV) open-reading frame (ORF) 29 gene product can act as a modulator of VZV gene expression. The ORF 29 protein alone does not appear to have any effect on transcription; however, in its presence, changes in the level of reporter gene activity mediated by the VZV immediate early (IE) 62 major transactivator are seen. Increased expression was observed in human fibroblasts, MeWo cells, HeLa cells, and T cells. In contrast, the presence of the ORF 29 protein results in a down-regulation of IE62 activation in PC-12 rat neuronal cells. Competition filter binding assays indicate that the ORF 29 protein binds specifically to the glycoprotein I promoter. Since transcripts for ORF 29 and ORF 62 have been detected in latently infected ganglia, the gene regulatory properties of the ORF 29 protein may be relevant to maintenance or establishment of VZV latency.
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