Search Results - (Author, Cooperation:M. R. Capobianchi)
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1M. W. Carroll ; D. A. Matthews ; J. A. Hiscox ; M. J. Elmore ; G. Pollakis ; A. Rambaut ; R. Hewson ; I. Garcia-Dorival ; J. A. Bore ; R. Koundouno ; S. Abdellati ; B. Afrough ; J. Aiyepada ; P. Akhilomen ; D. Asogun ; B. Atkinson ; M. Badusche ; A. Bah ; S. Bate ; J. Baumann ; D. Becker ; B. Becker-Ziaja ; A. Bocquin ; B. Borremans ; A. Bosworth ; J. P. Boettcher ; A. Cannas ; F. Carletti ; C. Castilletti ; S. Clark ; F. Colavita ; S. Diederich ; A. Donatus ; S. Duraffour ; D. Ehichioya ; H. Ellerbrok ; M. D. Fernandez-Garcia ; A. Fizet ; E. Fleischmann ; S. Gryseels ; A. Hermelink ; J. Hinzmann ; U. Hopf-Guevara ; Y. Ighodalo ; L. Jameson ; A. Kelterbaum ; Z. Kis ; S. Kloth ; C. Kohl ; M. Korva ; A. Kraus ; E. Kuisma ; A. Kurth ; B. Liedigk ; C. H. Logue ; A. Ludtke ; P. Maes ; J. McCowen ; S. Mely ; M. Mertens ; S. Meschi ; B. Meyer ; J. Michel ; P. Molkenthin ; C. Munoz-Fontela ; D. Muth ; E. N. Newman ; D. Ngabo ; L. Oestereich ; J. Okosun ; T. Olokor ; R. Omiunu ; E. Omomoh ; E. Pallasch ; B. Palyi ; J. Portmann ; T. Pottage ; C. Pratt ; S. Priesnitz ; S. Quartu ; J. Rappe ; J. Repits ; M. Richter ; M. Rudolf ; A. Sachse ; K. M. Schmidt ; G. Schudt ; T. Strecker ; R. Thom ; S. Thomas ; E. Tobin ; H. Tolley ; J. Trautner ; T. Vermoesen ; I. Vitoriano ; M. Wagner ; S. Wolff ; C. Yue ; M. R. Capobianchi ; B. Kretschmer ; Y. Hall ; J. G. Kenny ; N. Y. Rickett ; G. Dudas ; C. E. Coltart ; R. Kerber ; D. Steer ; C. Wright ; F. Senyah ; S. Keita ; P. Drury ; B. Diallo ; H. de Clerck ; M. Van Herp ; A. Sprecher ; A. Traore ; M. Diakite ; M. K. Konde ; L. Koivogui ; N. Magassouba ; T. Avsic-Zupanc ; A. Nitsche ; M. Strasser ; G. Ippolito ; S. Becker ; K. Stoecker ; M. Gabriel ; H. Raoul ; A. Di Caro ; R. Wolfel ; P. Formenty ; S. Gunther
Nature Publishing Group (NPG)
Published 2015Staff ViewPublication Date: 2015-06-18Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsPublished by: -
2Staff View
ISSN: 1432-8798Source: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Summary Replication kinetics of HIV was studied under single growth cycle conditions by backtitrating infectious virus released or remained cell-associated at each time point. Under these conditions HIV seems to replicate faster than previously estimated. The amount of cell-associated virus always exceeds the one detectable in the medium.Type of Medium: Electronic ResourceURL: -
3Staff View
ISSN: 1432-8798Source: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Summary The cellular source of IFN alpha after induction with Herpes simplex virus type-1 (HSV) and HSV-infected fibroblasts was investigated by using human peripheral blood mononuclear cell (PBMC) populations, purified according to conventional procedures, and which included T- and B-lymphocytes as well as monocytes. It appears that the cells responding to HSV virions are monocytes, whereas the PBMC population induced by HSV-infected cells is represented by B-lymphocytes. Furthermore, by using monoclonal antibody (MoAb) to HLA class I and class II products, it appears that different membrane structures are involved in the induction of IFN by HSV virions, as opposed to HSV-infected cells. In fact, most anti-HLA class II MoAbs inhibit IFN induction by HSV-infected cells, and not IFN induction by HSV virions.Type of Medium: Electronic ResourceURL: -
4Abbate, I. ; Capobianchi, M. R. ; Fais, S. ; Castilletti, C. ; Mercuri, F. ; Cordiali Fei, P. ; Ameglio, F. ; Dianzani, F.
Springer
Published 1995Staff ViewISSN: 1432-8798Source: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Summary HIV-1 acquires cell membrane proteins during budding. The cell membrane proteins (CMP) profile of laboratory HIV-1 strains grown in different host cells was established, by using an immobilized antibody capture (IAC), to verify whether CMPs present on HIV-1 correlate with its host cell origin. HIV-1 grown in different cell lines incorporates cell markers such as CD3, CD19, CD14, CD31 and IL 2-R, according to the distinctive expression of these antigens on the host cells. Furthermore, also T-tropic and monocytotropic HIV-1 strains display host cell specific markers, supporting the hypothesis that virus associated CMPs are a marker of host cell origin.Type of Medium: Electronic ResourceURL: -
5Staff View
ISSN: 1432-8798Source: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Summary We compared the properties of interferon (IFN) induced in peripheral blood mononuclear cells (PBMC) by free infectious HIV to that induced by HIV-infected cells fixed with glutaraldehyde. While the IFN induced by HIV was a conventional IFN alpha, the IFN induced by HIV-infected cells, although sharing with IFN alpha both antigenic properties and molecular weight, was strongly inactivated by treatment at pH lower than 4. The ability to induce acid-labile IFN alpha was exerted both by the chronically—infected cell line H9/HIV and by normal PBMC infected in vitro with HIV, while infection of inducers cells with viruses other than HIV made these cells capable of inducing only acid-stable IFN alpha. The cell involved in the production of this type of IFN seems to be B-lymphocyte. Because the presence of acid-labile IFN alpha in the serum of AIDS patients has been described, we suggest that this unusual IFN derives from interaction between circulating B-lymphocytes and the HIV-infected cells.Type of Medium: Electronic ResourceURL: -
6Scheglovitova, O. ; Scanio, V. ; Fais, S. ; Papadia, S. ; Abbate, I. ; Castilletti, C. ; Dianzani, F. ; Capobianchi, M. R.
Springer
Published 1995Staff ViewISSN: 1432-8798Source: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Summary Human umbilical vein endothelial cells (HUVEC) can be abortively infected with HIV-1, but virus production is rescued by the addition of T cells. Monoclonal antibody (Mab) to ICAM-1, but not its Fab' fragment or MAbs to LFA-1 and PECAM-1, increases HIV-1 infection of HUVEC by enhancing HIV-1 absorption. Enhancement by anti ICAM-1 is probably due to a bridging effect different from the ADE mediated by anti-gp120 that involves FcR or CR-mediated capture of the virus-antibody complex. Since antibodies to cell membrane molecules are present in HIV-1 infected patients, the ADE mediated by such a mechanism can be important in AIDS pathogenesis.Type of Medium: Electronic ResourceURL: -
7Scheglovitova, Olga ; Capobianchi, M. R. ; Antonelli, G. ; Guanmu, D. ; Dianzani, F.
Springer
Published 1993Staff ViewISSN: 1432-8798Source: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Summary Human primary endothelial cell cultures, derived from umbilical vein (HUVEC), can be infected by different strains of HIV-1, but mature virus production remains undetectable both in supernatants and in cellular extracts. Yet viral DNA is transiently detectable during the first days of infection, but progressively declines during the subsequent days. This finding is characteristic of abortive infections. Co-culture of HUVEC carrying HIV DNA with activated peripheral blood mononuclear cells or with CD 4-positive lymphoid cells elicited a massive cpe (syncytia formation and cell degeneration) in the latter cells, caused by the establishment of productive HIV-1 infection. HUVEC infected in the presence of AZT were significantly impaired in the ability to transmit the infection of CD 4-positive cells, indicating that active DNA synthesis is required in HUVEC before rescue by CD 4-positive cells. These results are of interest in view of the possibility that endothelial cells can play a role in the transmission of HIV-1 infection from infected pregnant women to the foetuses, and, more generally, suggest a potential role of endothelial cells as a transient reservoir of HIV-1.Type of Medium: Electronic ResourceURL: -
8Matricardi, P. M. ; Capobianchi, M. R. ; Paganelli, R. ; Facchini, J. ; Sirianni, M. C. ; Seminara, R. ; Dianzani, F. ; Aiuti, F.
Springer
Published 1984Staff ViewISSN: 1573-2592Keywords: Immunodeficiency ; gamma-interferon ; alpha-interferon ; monoclonal antibodiesSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Abstract Alpha- and gamma-interferon (IFN) production by peripheral blood mononuclear cells (PBMC) from 18 patients affected by primary immunodeficiency syndromes was examined and compared with that of 20 normal donors. Patients included 8 with common variable immunodeficiency (CVI), 2 with congenital agammaglobulinemia, 4 with ataxia-telangiectasia, 2 with hyper-IgE syndrome, 1 with chronic EBV infection, 1 with combined immunodeficiency, and 1 with immunodeficiency with hyper-IgM. No spontaneous IFN production was observed in either patients and controls. Newcastle disease virus-induced alpha-IFN production was found to be normal in all patients. Gamma-IFN was induced by both galactose oxidase and staphylococcal enterotoxin (B). Gamma-interferon production was low or undetectable in patients with ataxia-telangiectasia, in immunodeficiency with hyper-IgM, and in hyper-IgE syndrome. No major defect of gamma-IFN was found in other types of immunodeficiency, despite the presence of occasional low producers (1 of 8 CVI patients and 1 case of congenital agammaglobulinemia). No correlation was found between IFN production and natural killer activity in individual patients. The analysis of lymphocyte subsets by monoclonal antibodies revealed gross imbalances of helper/inducer and suppressor/cytotoxic subpopulations, but no overall correlation could be established with gamma-IFN production. The observation of major defects in gamma-IFN yield only in diseases with depression of T cell-mediated immunity might contribute to a better understanding of the pathogenetical mechanisms in these diseases. Moreover, future studies should monitor thesein vitro functions and their modifications byin vitro orin vivo manipulations.Type of Medium: Electronic ResourceURL: