@article{GowSimpsonSchliephakeetal.1992,
  author    = {Gow, J. W. and Simpson, K. and Schliephake, Andreas and Behan, W. M. and Morrison, L. J. and Cavanagh, H. and Rethwilm, Axel and Behan, P. O.},
  title     = {Search for retrovirus in the chronic fatigue syndrome},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-61436},
  year      = {1992},
  abstract  = {Aim: To examine peripheral blood and skeletal muscle from patients with chronic fadgue syndrome for exogenous retrovirus. Methods: Blood samples from 30 patients and muscle biopsy specimens of 15 patients were examined for retroviral sequences by DNA extraction, polymerase chain reacdon (PCR), and Southern blotting hybridisation. Sera were examined for human foamy virus by western immunoblotting and indirect immunofluorescence techniques. Results: No difference between the padent and control populations was found for any of the PCR primer sets used (gag, pol, env, and tax regions of HTLV VII). An endogenous gag band was observed in both the padent and control groups. All sera were negative for antibody to human foamy virus. Conclusion: The results indicate that there is no evidence of retroviral involvement in the chronic fatigue syndrome.},
  subject      = {Virologie},
  language  = {en}
}
@article{JaffeyChanShaoetal.1992,
  author    = {Jaffey, P. and Chan, L.-N. L. and Shao, J. and Schneider-Schaulies, J{\"u}rgen and Chan, T.-S.},
  title     = {Retinoic acid inhibition of serum-induced c-fos transcription in a fibrosarcoma cell line},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-54863},
  year      = {1992},
  abstract  = {No abstract available},
  subject      = {Immunologie},
  language  = {en}
}
@article{KerkauGernertKneitzetal.1992,
  author    = {Kerkau, T. and Gernert, S. and Kneitz, C. and Schimpl, A.},
  title     = {Mechanism of MHC class I downregulation in HIV infected cells},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-56849},
  year      = {1992},
  abstract  = {HIV infection of CD4+ peripheral blood lymphocytes leads to a loss of MHC dass I molecules on the surface of the infected cells as detectable by monodonal antibody staining and flow cytometry. Incubation of the infected cells at 26 oe or treatment at 37 oe with peptides leads to upregulation of MHC dass I to levels equal to those found on uninfected cells cultured und er the same conditions. The data suggest that, after HIV infection, the mechanisms responsible for peptide generation, peptide transport and thus stable association between peptides and MHC dass I molecules are severely affected.},
  subject      = {HIV},
  language  = {en}
}
@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{AguzziBothAnhauseretal.1992,
  author    = {Aguzzi, A. and Both, K. and Anhauser, I. and Horak, I. and Rethwilm, Axel and Wagner, EF.},
  title     = {Expression of human foamy virus is differentially regulated during development in transgenic mice},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-55290},
  year      = {1992},
  abstract  = {Tbe human foamy virus (HFV) is a recently characterized member ofthe spumavirus family. Although no diseases have been unequivocally associated with HFV infection, expression of HFV regulatory genes in transgenie mice induces a characteristic aeute neuro degenerative disease and a myopathy. To better eharaeterize the sequenee of events leading to disease, and to gain a better understanding of the underlying pathogenetic meehanisms, we have analyzed in detail the transgene expression pattern during development. Transcription of a construet containing all regulatory elements and aneillary genes of mv was analyzed by in situ hybridization and was shown to occur in two distinct phases. At midgestation, low but widespread expression was first deteeted in eells of extraembryonie tissues. Later, various tissues originating from embryonie mesoderm, neuroeetoderm, and neural erest transeribed the transgene at moderate levels. However, expression deereased dramatically during late gestation and was suppressed shortly after birth. After a latency period of up to 5 weeks, transeription of the transgene resumed in single eelJs distributed irregularly in the central nervous system and in the skeletal museIe. By the age of 8 weeks, an increasing number of eells displayed much higher expression levels than in embryonie Iife and eventually underwent severe degenerative ehanges. These findings demonstrate that HFV transgene expression is differentially regulated in development and that HFV cytotoxicity may be dose-dependent. Such biphasic pattern of expression differs from that of murine retroviruses and may be explained by the specificity of HFV regulatory elements in combination with cellular faetors. Future studies of this model system should, therefore, provide novel insights in the mechanisms controlling retrovirallatency.},
  subject      = {Virologie},
  language  = {en}
}
@article{SchneiderSchauliesLiebertRagerZismanetal.1992,
  author    = {Schneider-Schaulies, Sibylle and Liebert, U. G. and Rager-Zisman, B. and Wolfson, M. and ter Meulen, V.},
  title     = {Antibody-dependent transcriptional regulation of measles virus in persistently infected neural cells},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-62329},
  year      = {1992},
  abstract  = {No abstract available},
  subject      = {Virologie},
  language  = {en}
}