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Correlation between p19 presence and MHC class II expression in human fetal astroglial cells cocultured with HTLV‐I donor cells
Author(s) -
Macchi B.,
Caronti B.,
Cocchia D.,
Gremo F.,
Torelli S.,
Sogos V.,
Bonmassar E.,
Lauro G.M.
Publication year - 1992
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/0736-5748(92)90063-6
Subject(s) - tropical spastic paraparesis , biology , glial fibrillary acidic protein , in vitro , microbiology and biotechnology , cell culture , antigen , virology , astrocyte , cytopathic effect , immunology , mhc class i , virus , cell , major histocompatibility complex , neuroscience , myelopathy , spinal cord , central nervous system , genetics , immunohistochemistry
The possibility of a direct infection of human brain by HTLV‐I, has been studied using an in vitro model. Human fetal astroglial cells were cocultivated with irradiated HTLV‐I donor cell line MT‐2, and assayed for the presence of HTLV‐I core protein p19 after 1 week. Fifty‐six per cent of GFAP positive astrocytes showed the viral core protein p19 and increased expression of Class II MHC antigens. Electron microscopy of astroglial cells exposed to HTLV‐I revealed the presence of vacuoli‐like structures containing viral core protein p19. Cell intermediate filament cytoskeleton was also disorganized. Even if this study does not provide direct evidence for virus replication inside astroglial cells, all these findings suggest that HTLV‐I can indeed enter the cell and exert a cytopathic effect. Therefore the results of the present study are consistent with the hypothesis that astroglial cells could be involved in demyelination processes occurring in the HTLV‐I associated neurological disorders, such as human associated myelopathy and tropical spastic paraparesis.