- HOME
- Vol.45 No.11
- CLINICA NEUROL, 45: 815－817, 2005
- Vol.45 No.11 contents
The 46th Annual Meeting of the Japanese Society of Neurology
Retrovirus infection and neurological disorders
Shuji Izumo, M.D.
Division of Molecular Pathology, Center for Chronic Viral Diseases, Graduate School of Medical and Dental Sciences, Kagoshima University
Our series of neuropathologic studies on HAM/TSP and AIDS dementia were reviewed. Studies on HAM/TSP demonstrated chronic inflammatory process in the spinal cord, accentuated inflammation in the area with slow blood flow in the spinal cord, characteristic adhesion molecule expression for T-cell migration, apoptosis of helper T-cells in active inflammatory lesion, correlation of HTLV-I provirus amount with disease activity, and HTLV-I infection and expression of HTLV-I gene on infiltrated T-cells in the spinal cord lesion. Based on these findings, we have proposed a by-stander mechanism as a pathogenesis of HAM/TSP.
HIV-1 also involves the CNS, however, its pathogenesis has not been fully studied yet. To understand the pathogenesis of AIDS dementia, we used a SIV-macaque model and demonstrated that there are two independent pathogenic processes in AIDS dementia; AIDS-dependent neuropil degeneration in the cortex caused by T-cell tropic virus, and immune response against invading virus-infected cells in the white matter caused by macrophage tropic virus. The latter mechanism is similar to that of HAM/TSP. Invasion of virus-infected blood cells inside the CNS and a gradual damage of surrounding CNS tissues caused by prolonged immune attack to these virus-infected cells may be a common pathogenic process of retrovirus induced CNS diseases.
(CLINICA NEUROL, 45: 815－817, 2005)
key words: HTLV-I associated myelopathy (HAM), AIDS encephalopathy, pathogenesis, Neuropathology
(Received: 25-May-05)
