@article{SchneiderSchauliesSchneiderSchauliesBrinkmannetal.1992,
  author    = {Schneider-Schaulies, J{\"u}rgen and Schneider-Schaulies, Sibylle and Brinkmann, R. and Tas, P. and Halbr{\"u}gge, M. and Walter, U. and Holmes, H.C. and ter Meulen, Volker},
  title     = {HIV-1 gp120 receptor on CD4-negative brain cells activates a tyrosine kinase},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-54872},
  year      = {1992},
  abstract  = {Human immunodeficiency virus (HIV-1) infection in the human brain Ieads to characteristic neuropathological changes, which may result indirectly from interactions of the envelope glycoprotein gp 120 with neurons and/or glial cells. We therefore investigated the binding of recombinant gp120 (rgp120) to human neural cells and its effect on int~acellular.s.ignallin~. Herewe pre~ent evidence that rgp120, besides binding to galactocerebroside or galactosyl-sulfatlde, spec1f1cally bmds to a protem receptor of a relative molecular mass of approximately 180,000 Da (180 kDa) pre~ent. on the CD4-negative glioma cells D-54, but not on Molt4 T lymphocytes. Binding of rgp120 to this receptor rap1dly 1nduced a tyrosine-specific protein kinase activity leading to tyrosine phosphorylation of 130- and 115-kDa p~oteins. The c~ncentration of intracellular calciumwas not affected by rgp120 in these cells. Our data suggest a novel Signal transduc1ng HIV-1 gp120 receptor on CD4-negative glial cells, which may contribute to the neuropathological changes observed in HIV-1-infected brains.},
  subject      = {Immunologie},
  language  = {en}
}
@article{BrinkmannSchwinnMuelleretal.1993,
  author    = {Brinkmann, R. and Schwinn, A. and M{\"u}ller, J. and Stahl-Hennig, C. and Coulibaly, C. and Hunsmann, G. and Czub, S. and Rethwilm, Axel and D{\"o}rries, R. and ter Meulen, Volker},
  title     = {In vitro and in vivo infection of rhesus monkey microglial cells by simian immunodeficiency virus},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-61415},
  year      = {1993},
  abstract  = {The observation that microglial cells in brain tissue are probably a major target for human immunodeficiency virus (HIV) infection has raised interest in the pathogenic role of this cell population for the development of neuro-AIOS. Since it is very difficult to obtain microglia from normal or diseased human brain we studied microglial cells isolated from fresh brain tissue of uninfected and simian immunodeficiency virus (SIV) infected rhesus monkeys (Macacca mulatta) in comparison to peripheral blood macrophages. Besides the characterization of the phenotypes of these two cell populations, we examined the replication of SIV in the cells in addition to the effect of viral infection on the expression of cell surface molecules. We found that microglia and macrophages support replication of the wild-type SIV\(_{mac25}\), strain as well as the infectious clone (SIV\(_239\)). Infectious viruswas produced and a CPE developed. Isolated microglial cells from SIV-infected monkeys were latently infected independent of the presence of neuropathological lesions and produced infectious virus after 20-25 days in culture. In situ hybridization revealed that only a small percentage of isolated microglial cells are productively infected in vivo, yet the majority of these expressed MHC class II molecules. This indicated a state of activation that is acquired in vivo. These findings indicate that microglia are a prime target cell for SIV infection in CNS tissue.},
  subject      = {Virologie},
  language  = {en}
}