[Retrovirus infection and neurological disorders].
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.
Izumo
Shuji
S
Division of Molecular Pathology, Center for Chronic Viral Diseases, Graduate School of Medical and Dental Sciences, Kagoshima University.
D015526:AIDS Dementia Complex / Q000473:pathology / Q000821:virology; D015368:Human T-lymphotropic virus 1 / Q000302:isolation & purification; D006801:Humans; D009422:Nervous System Diseases / Q000209:etiology; D015493:Paraparesis, Tropical Spastic / Q000276:immunology / Q000473:pathology / Q000821:virology; D012192:Retroviridae Infections / Q000150:complications