@article{RiedererterMeulen2020,
  author    = {Riederer, Peter and ter Meulen, Volker},
  title     = {Coronaviruses: a challenge of today and a call for extended human postmortem brain analyses},
  series = {Journal of Neural Transmission},
  volume    = {127},
  journal   = {Journal of Neural Transmission},
  number    = {9},
  issn      = {0300-9564},
  doi       = {10.1007/s00702-020-02230-x},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-314637},
  pages     = {1217-1228},
  year      = {2020},
  abstract  = {While there is abounding literature on virus-induced pathology in general and coronavirus in particular, recent evidence accumulates showing distinct and deleterious brain affection. As the respiratory tract connects to the brain without protection of the blood-brain barrier, SARS-CoV-2 might in the early invasive phase attack the cardiorespiratory centres located in the medulla/pons areas, giving rise to disturbances of respiration and cardiac problems. Furthermore, brainstem regions are at risk to lose their functional integrity. Therefore, long-term neurological as well as psychiatric symptomatology and eventual respective disorders cannot be excluded as evidenced from influenza-A triggered post-encephalitic Parkinsonism and HIV-1 triggered AIDS-dementia complex. From the available evidences for coronavirus-induced brain pathology, this review concludes a number of unmet needs for further research strategies like human postmortem brain analyses. SARS-CoV-2 mirroring experimental animal brain studies, characterization of time-dependent and region-dependent spreading behaviours of coronaviruses, enlightening of pathological mechanisms after coronavirus infection using long-term animal models and clinical observations of patients having had COVID-19 infection are calling to develop both protective strategies and drug discoveries to avoid early and late coronavirus-induced functional brain disturbances, symptoms and eventually disorders. To fight SARS-CoV-2, it is an urgent need to enforce clinical, molecular biological, neurochemical and genetic research including brain-related studies on a worldwide harmonized basis.},
  language  = {en}
}
@article{SchneiderSchauliesSchneiderSchauliesterMeulen1993,
  author    = {Schneider-Schaulies, J{\"u}rgen and Schneider-Schaulies, S. and ter Meulen, Volker},
  title     = {Differential induction of cytokines after primary and persistent measles virus infections of human glial cells},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-54907},
  year      = {1993},
  abstract  = {The effect of measles virus (MV) infection on mRNA expression and protein synthesis of cytokines in human malignant glioma celllines (0-54 and U-251) was investigated. Primary MV infections led in both celllines to the induction of interleukin-1 fJ (ll-1 (3), interleukin-6 (IL-6), interferon-(3 (IFN-fJ), and tumor necrosis factor-a (TNF-a). ln contrast, persistently infected astrocytoma lines continually produced IL-6 (two out of 12 lines high Ievels) and IFN-ß, whereas only 1 out of 121ines synthesized TNF-a and none IL-1ß. The pathways for induction of IL-1fJ and TNF-a expression were not suppressed by the persistent MV infection, since IL-1ß and TNF-a could be induced by external stimuli Jike diacylglycerol analog plus calcium ionophore. lnterestingly, persistently infected astrocytoma cells synthesized considerably higher Ievels of ll-1ß and TNF-a than uninfected cells afteradditional external induction. These results suggest that in the centrat nervous system (CNS) of SSPE patients a percentage of persistently infected astrocytes may continually synthesize IL-6 and IFN-ß, and in the presence of additional external stimuli, as possibly provided by activated lymphocytes, might ovarexpress the inflammatory cytokines IL-1 ß and TNF-a. This may be of pathogenetic significance in CNS diseases associated with persistent MV infections.},
  subject      = {Immunologie},
  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{NetzerRethwilmMaureretal.1990,
  author    = {Netzer, Kai O. and Rethwilm, Axel and Maurer, Bernd and ter Meulen, Volker},
  title     = {Identification of the major immunogenic structural proteins of human foamy virus},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-61477},
  year      = {1990},
  abstract  = {We have identified the major immunogenic structural proteins of the human foamy virus (HFV), a distinct member of the foamy virus subfamily of Retroviridae. Radiolabelied viral proteins were immunoprecipitated from HFV -infected cells by foamy virus antisera of human and non-human primate origin. Precipitated viral proteins were in the range of 31 K to 170K. Labelling of proteins with [\(^{14}\)C]glucosamine or with [\(^{35}\)S]methionine in the presence oftunicamycin, as well as endo-ß-N-acetylglycosaminidase Hand F treatment of [\(^{35}\)S]methionine-labelled proteins, revealed three viral glycoproteins of approximately 170K, 130K and 47K, most likely representing the env gene-encoded precursor, the surface glycoprotein and the transmembrane protein of HFV, respectively.},
  subject      = {Virologie},
  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}
}
@article{SchneiderSchauliesLiebertBaczkoetal.1988,
  author    = {Schneider-Schaulies, Sibylle and Liebert, U. G. and Baczko, K. and ter Meulen, Volker},
  title     = {Molecular Biological Analyses of Measles Virus Gene Expression in the CNS of Acutely and Persistently Infected Rat Brain Cells},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-34104},
  year      = {1988},
  abstract  = {No abstract available},
  subject      = {Masernvirus},
  language  = {en}
}
@article{JocherRethwilmKapposetal.1990,
  author    = {Jocher, R. and Rethwilm, Axel and Kappos, L. and ter Meulen, Volker},
  title     = {Search for retroviral sequences in peripheral blood mononuclear cells and brain tissue of multiple sclerosis patients},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-61462},
  year      = {1990},
  abstract  = {DNAs from peripheral blood mononuclear cells (PBMCs) of 21 patients with multiple sclerosis (MS), 1 patient with tropical spastic paraparesis (TSP) as well as DNAs from brain and spinal cord of 5 MS cases and 3 controls were examined for human T-cell lymphotropic virus (HTLV)-related sequences by polymerase chain reaction. The primers used were derived from the HTLV-1 gag, env and tax genes. Amplified products were separated on agarase gels, blotted onto nylon membranes and hybridized to specific radiolabelled oligonucleotides. The sensitivity of amplification and hybridization was one copy of target DNA in 10\8^5\) cellular genomes. None of the specimens was positive for HTLV-1 sequences except the TSP probe. These negative data are all the more significant because brain -material from MS patients was used in these studies. Our studies thus fail to support speculations that HTLV-I is involved in the aetiology of multiple sclerosis.},
  subject      = {Virologie},
  language  = {en}
}
@article{SchneiderSchauliesSchnorrDunsteretal.1994,
  author    = {Schneider-Schaulies, Sibylle and Schnorr, J.-J. and Dunster, L. M. and Schneider-Schaulies, J{\"u}rgen and ter Meulen, Volker},
  title     = {The role of host factors in measles virus persistence},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-54944},
  year      = {1994},
  abstract  = {As critical steps in the life cycle oJ measles virus (Mfl), the e.fficiency of uptake into and replication in susceptible host cells are governed by cellular determinants. Measles virus infections of cells of the human CNS are characterized by particular constraints imposed on v1:ral transcription and translation attenuating viral gene Junctions and thus contributing to the pathogenesis oJ MV persistence in these cells.},
  subject      = {Immunologie},
  language  = {en}
}
@article{MuellerKrennCzubetal.1993,
  author    = {M{\"u}ller, J. and Krenn, V. and Czub, S. and Schindler, C. and Kneitz, C. and Kerkau, T. and Stahl-Henning, C. and Coulibaly, C. and Hunsmann, G. and Rethwilm, Axel and ter Meulen, Volker and M{\"u}ller-Hermelink, H. K.},
  title     = {The thymus in SIV infection},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-80265},
  year      = {1993},
  abstract  = {no abstract available},
  subject      = {HIV-Infektion},
  language  = {en}
}
@article{RethwilmErlweinBaunachetal.1991,
  author    = {Rethwilm, Axel and Erlwein, Otto and Baunach, Gerald and Mauerer, Bernd and ter Meulen, Volker},
  title     = {The transcriptional transactivator of human foamy virus maps to the bel 1 genomic region},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47342},
  year      = {1991},
  abstract  = {The human foamy virus (HFV) genome possesses three open reading frames (bel I, 2, and 3) located between env and the 3' long terminal repeat. By analogy to other human retroviruses this region was selected as the most Iikely candidate to encode the viral transactivator. ResuIts presented here confirmed this and showed further that a deletion introduced only into the bell open reading frame of a plasmid derived from an infectious molecular clone of HFV abolished transactivation. In contrast, deletions in bel 2 and bel 3 had only minor effects on the ability to transactivate. The role of the bel I genomic region as a transactivator was further investigated by eukaryotic expression of a genome fragment of HFV spanning the bel I open reading frame. A construct expressing bell under control of a heterologous promoter was found to transactivate the HFV long terminal repeat in a dose-dependent fashion. Furthermore, it is shown that the U3 region of the HFV long terminal repeat is sufficient to respond to the HFV transactivator.},
  subject      = {Virologie},
  language  = {en}
}