An enzyme immunoassay (EIA) was developed for detection of Human T-cell Leukemia Virus antigen in culture supernatants and cell lysates. The assay used a mouse monoclonal antibody against HTLV-I pl9 major core protein as capture antibody. It has a sensitivity of lμ.g/ml of HTLV-I protein, 250pg/ml of purified recombinant pl9 and detected pl9 in an 10-2 diluted supernatant of MT2 infected cell and in a 100 MT2 cells lysate (106 cells taken at day 7 of culture). The assay enable us to discriminate between HTLV-I and HTLV-II antigens and is reproductively negative for supernatants and cell lysates of uninfected cells and of HIV-1 infected cells. The assay was found to be more specific and 10 times more sensitive than the reverse transcriptase (RT) assay, and the EIA test became positive three days earlier than RT assay for the HTLV-I cell lines supernatants.
Journal Article Regeneration of the antivirel drug (E) -5-(2-bromovinyl)-2′ -deoxyuridine in vivo Get access Claude Desgranges, Claude Desgranges *unité 8 de Cardiologie de I'INSERMAvenue du Haut-Levèque, 33600 Pessac, France+Institute for Medical Research, Katholieke Universiteit LeuvenMinderbroedersstraat 10, B-3000 Leuven, Belgium Search for other works by this author on: Oxford Academic PubMed Google Scholar Gabriel Razaka, Gabriel Razaka *unité 8 de Cardiologie de I'INSERMAvenue du Haut-Levèque, 33600 Pessac, France Search for other works by this author on: Oxford Academic PubMed Google Scholar Françoise Drouiller, Françoise Drouiller *unité 8 de Cardiologie de I'INSERMAvenue du Haut-Levèque, 33600 Pessac, France Search for other works by this author on: Oxford Academic PubMed Google Scholar Henri Bricaud, Henri Bricaud *unité 8 de Cardiologie de I'INSERMAvenue du Haut-Levèque, 33600 Pessac, France Search for other works by this author on: Oxford Academic PubMed Google Scholar Piet Herdewijn, Piet Herdewijn +Institute for Medical Research, Katholieke Universiteit LeuvenMinderbroedersstraat 10, B-3000 Leuven, Belgium Search for other works by this author on: Oxford Academic PubMed Google Scholar Erik De Clercq Erik De Clercq +Institute for Medical Research, Katholieke Universiteit LeuvenMinderbroedersstraat 10, B-3000 Leuven, Belgium Search for other works by this author on: Oxford Academic PubMed Google Scholar Nucleic Acids Research, Volume 12, Issue 4, 24 February 1984, Pages 2081–2110, https://doi.org/10.1093/nar/12.4.2081 Published: 24 February 1984 Article history Received: 05 January 1984 Accepted: 23 January 1984 Published: 24 February 1984
Estradiol (E(2)) is known to accelerate reendothelialization and thus prevent intimal thickening and in-stent restenosis after angioplasty. Transplantation experiments with ERalpha(-/-) mice have previously shown that E(2) acts through local and bone marrow cell compartments to enhance endothelial healing. However, the downstream mechanisms induced by E(2) to mediate endothelial repair are still poorly understood.We show here that after endovascular carotid artery injury, E(2)-enhanced endothelial repair is lost in osteopontin-deficient mice (OPN(-/-)). Transplantation of OPN(-/-) bone marrow into wild-type lethally irradiated mice, and vice versa, suggested that osteopontin plays a crucial role in both the local and the bone marrow actions of E(2). In the vascular compartment, using transgenic mice expressing doxycyclin regulatable-osteopontin, we show that endothelial cell specific osteopontin overexpression mimics E(2)-enhanced endothelial cell migration and proliferation in the regenerating endothelium. In the bone marrow cell compartment, we demonstrate that E(2) enhances bone marrow-derived mononuclear cell adhesion to regenerating endothelium in vivo, and that this effect is dependent on osteopontin.We demonstrate here that E(2) acceleration of the endothelial repair requires osteopontin, both for bone marrow-derived cell recruitment and for endothelial cell migration and proliferation.
Abstract Fifty‐six South Chinese individuals exhibiting IgA antibodies to EBV for 18 months and presenting naso‐pharyngeal abnormalities were biopsied. Four nasopha‐ryngeal carcinomas, two at a very early stage, were detected. In 14 further individuals, without clinical or his‐topathological evidence of tumor, EBV/DNA internal repeats and/or EBNA were detected in the biopsied mucosae. The presence of IgA/EBV antibodies and/or EBV markers in the nasopharyngeal mucosa may characterize pre‐cancerous conditions.
Abstract Previous studies based on the use of human serum as a source of C have provided evidence for the C-dependent enhancement of cell infection by HIV-1. The present study was undertaken to distinguish C from other serum factors and to identify the proteins and the mechanisms involved in C-dependent cell infection by HIV-1. The classical C activation pathway was reconstituted from the proteins C1q, C1r, C1s, C4, C2, C3, factor H, and factor I; each were purified to homogeneity. A mixture of these proteins at physiological concentrations was shown to reproduce the ability of normal human serum to enhance the infection of MT2 cells by HIV-1 at low doses of virus. This enhancing effect was abolished when heat-inactivated serum and C2- or C3-depleted serum were used, and was restored upon addition of the corresponding purified proteins. A mixture of two synthetic peptides corresponding to positions 10–15 and 90–97 of human C receptor type 2 (CD21) as well as soluble CD4 both inhibited the C-dependent infection process. These data provide unambiguous evidence that HIV-1 triggers a direct activation of the classical C pathway in vitro and thereby facilitates the infection of MT2 cells at low doses of virus. These findings are consistent with a mechanism involving increased interaction between the virus opsonized by C3b-derived fragment(s) and the CD21 cell receptors and subsequent virus entry through CD4 receptors.
