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Biomedical subjects

L Thiry

Publications and source records attributed to L Thiry.

At least 37 records · Page 2Linked to original sources
PubMed1986

Glycosylation inhibitors block the expression of LAV/HTLV-III (HIV) glycoproteins.

The glycosylation inhibitors 2-deoxy-D-glucose (2-dGlc) and, to a lesser extent, beta-hydroxynorvaline blocked the formation of syncytia in HIV (LAV/HTLV-III)-infected cells. Using monospecific polyclonal antibodies against recombinant envelope proteins gp110 and gp41 or monoclonal antibodies against env gp110, we could demonstrate a marked reduction in the immunoreactivity of these antigens in HIV-infected cells exposed to the glycosylation inhibitors. There was concomitant accumulation of core proteins p15 and p24, as shown by a solid phase radio-immunoassay, and a decreased oligosaccharide synthesis of env proteins, as monitored by the incorporation of [6-3H]GlcNAc. The reverse transcriptase was not affected by the compounds. Glycosylation inhibitors may be considered for the chemotherapy of AIDS or AIDS-related complex, or chemoprophylaxis of HIV-positive individuals.

Deoxy Sugars↗
PubMed1986

Markers of HTLV-III in patients with end stage renal failure treated by haemodialysis.

Patients and members of staff from a haemodialysis unit were tested for markers of infection with human T cell lymphotropic virus type III (HTLV-III), the virus associated with the acquired immune deficiency syndrome (AIDS). An enzyme linked immunosorbent assay showed eight of 100 patients to have antibodies to HTLV-III. In five of these patients past or present infection with HTLV-III was confirmed by Western blot analysis or detection of HTLV-III antigens in lymphocyte cultures, or both. Investigation of other risk factors for AIDS showed that the putative source of HTLV-III was unrelated to dialysis in two patients whereas blood transfusion was the most likely cause of contamination in the others. No member of staff gave a positive result in the enzyme linked immunosorbent assay. Nosocomial transmission of HTLV-III seems unlikely if precautions similar to those recommended for the control of hepatitis B infection are applied.

Acquired Immunodeficiency Syndrome↗
PubMed1986

LAV/HTLV-III infection in children of African origin: experience in Belgium.

From December 1982 to June 1985, we diagnosed LAV/HTLV-III infection in 16 children of African origin living in Belgium or referred to one of the hospitals participating in this study. Diagnosis was proven in seven of them by isolation of virus of the LAV/HTLV-III group. In the nine others, LAV/HTLV-III infection was highly probable because of the presence of antibodies against the virus (seven subjects) or clinical and immunological evidence of immune deficiency associated with a parental history of LAV/HTLV-III infection (two subjects). Five of these children had a severe illness starting in the first months of life (range 20 days--4 months) and died within 4 months (range 19 days--10 months). Eight children presented later in life (mean age 35 months, range 2-66 months) with a milder and more chronic disease characterized by the presence of generalized lymphadenopathy (6/8), hepatomegaly (5/8), splenomegaly (5/8), interstitial pulmonary infiltration (4/8), parotid swelling (3/8), CSF lymphocytosis (3/5), diarrhoea without pathogen isolated (1/8) and fever (1/8). At least one of the parents of each child was of African origin. At the time of birth of their child two mothers and one father had an AIDS-related complex. After a mean period of 34 months (range 3-87 months) five fathers and six mothers had a symptomatic LAV/HTLV-III infection (AIDS or AIDS-related complex).

Acquired Immunodeficiency Syndrome↗
PubMed1985

Bovine leukemia virus-related antigens in lymphocyte cultures infected with AIDS-associated viruses.

An earlier finding that lymphocytes from African patients with the acquired immune deficiency syndrome (AIDS) react with rabbit antiserum to purified antigens of bovine leukemia virus (BLV) prompted a study of the possible cross-reactions between a BLV-infected ovine cell line and human lymphocytes inoculated with a strain of lymphadenopathy syndrome-associated virus (LAV). A solid-phase radioimmunoassay was used to detect antigenic markers of the retroviruses. Crude extracts from short-term cultures of lymphocytes infected with LAV bound rabbit antisera to the LAV glycoprotein gp13 (molecular weight 13,000) and the BLV proteins p24 and gp51, but did not bind antibodies to the p24 of human T-cell leukemia virus type I (HTLV-I). Antiserum to LAV gp13 reacted with an ovine cell line producing BLV but also weakly with virus-free ovine cells. Lymphocyte cultures from four African patients with AIDS expressed BLV-related antigens within 6 to 10 days of culture, at the moment when particle-bound reverse transcriptase was produced. BLV-related antigens were induced in lymphocyte cultures from healthy individuals by addition of filtered supernatant or irradiated cells of the original culture. The antisera to BLV used in this study may prove useful for the detection of AIDS-associated viruses in short-term cultures of lymphocytes from AIDS patients or their contacts.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Human syncytiotrophoblast membrane proteins defined using a heterologous antiserum.

Detergent extracts of human trophoblast plasma membranes (TrPM) and of other fetal tissues from the same conceptus were prepared and the proteins separated by use of isoelectric focusing. A major band of isoelectric point (pI) 4.1 was present in TrPM together with minor bands of (pI) 4.9, 5.9, 7.3, 7.8 and 7.9. These bands were absent from non-trophoblastic fetal tissues. The pI 4.1 protein reacted with an 125I-labelled IgG fraction of a heterologous antiserum raised against TrPM and was found to have an apparent molecular weight of 100,000. This protein did not appear to be placental alkaline phosphatase, SP1, transferrin or human chorionic gonadotrophin. Many neoplastic cell lines tested also revealed a major protein band of pI 4.1 but it has not been established that this was the same protein as found in the TrPM preparations.

Antigens, Surface↗
PubMed1984

Study of the expression of a glycoprotein of retroviral origin in the plasma of patients with hematologic disorders and in the plasma of normal individuals.

A 74,000 molecular weight glycoprotein was purified from the plasma of a patient with chronic myelogenous leukemia in blast crisis. Monoclonal antibodies were produced in the mouse and used to characterize this protein. It was shown to contain p15E antigenic determinants and portions of a reverse transcriptase. The level of this protein was found to be elevated in leukemic patients with high white blood cell counts and also in some patients with other hematopoietic disorders as compared to the level measured in normal individuals. The level of the protein was strongly reduced in acute leukemia patients after intense chemotherapy treatment. We tentatively conclude that this protein is of endogenous retroviral origin and perhaps regulates hematopoietic tissues.

Acute Disease↗
PubMed1983

Cell receptors for baboon endogenous virus recognized by monoclonal antibodies.

Hybridomas from mice immunized with baboon endogenous virus (BaEV) from A204(M7) cells produced several antiviral monoclonal antibodies and, in addition, antibodies D-12 and E-4, which appeared to be virus specific because they reacted with BaEV but not with Mason-Pfizer virus or RD-114 virus. However, they also bound to human virus-free cells, and they did not recognize BaEV from bat or canine host cells. Cell membrane targets for these antibodies comigrated with an 18,000-dalton protein, which may contain specific determinants of BaEV receptors since antibody masking of these cell sites prevented BaEV but not Mason-Pfizer virus or RD-114 virus adsorption. However, RD-114 virus interfered with BaEV adsorption. Thus, the two viral receptors must be adjacent, but the antibody D-12 and E-4 targets are not within the active site of RD-114 virus receptor. Conversely, cell coating with BaEV from bat or canine hosts inhibited antibody D-12 binding. Noncultivated human lymphocytes and cells from fetal organs bound much less antibody D-12 than did cells from established cell lines, with a correlation between amounts of antibody D-12 acceptor sites and BaEV receptors. Thus, in vivo, BaEV infection of human cells may be inefficient. In vitro, antibody D-12 treatment of chronically infected A204(M7) cells caused intracellular accumulation of viral proteins and decreased virus release, with no such effect on RD-114 virus-producing cells. Canine cells bound antibody D-12 only if coated with BaEV from A204(M7) cells, indicating that the human determinant coadsorbed with the virions to animal cells. Possibly, determinants of cell receptors participate in BaEV maturation and become associated with the virions.

Adsorption↗
PubMed1982

Monoclonal antibodies against baboon endogenous virus and against host cell antigens.

Monoclonal antibodies were produced by murine hybridomas after immunization with semipurified baboon endogenous virus. In a solid-phase radioimmunoassay, two antibodies (F12-9 and B9-18) reacted with viral antigen only. The antibodies A6-8 and C9-12 also reacted with virus-producing cells but not with control cells, whereas antibodies E4-6 and D12-2 bound to virus-free cells as well. The cytofluorometry technique confirmed these results and showed a competition between antibodies A6-8 and C9-12 for binding to virus-producing cells as well as a competition between antibodies D12-2 and E4-6 for binding to virus-free human cells. An immune precipitation assay with disrupted virions indicated that antibodies A6-8, B9-18, and C9-12 were directed against the gp70 glycoprotein, and that antibody F12-9 reacted with a viral antigen with a molecular weight of 18,000. The syncytia induced in RSa cells by baboon molecular weight of 18,000. The syncytia induced in RSa cells by baboon endogenous virus could be inhibited either when antibody A6-8 or C9-12 was combined to the virus or when the RSa cells were treated with the anticellular antibody D12-2 or E4-6. These two effects were not observed with Mason-Pfizer virus. Thus, of three antibodies with specificities for viral gp70, two (A6-8 and C9-12) were directed at viral sites responsible for syncytium formation. Another antiviral antibody (F12-9) reacted with a protein of unknown function with a molecular weight of 18,000. The two anticellular antibodies were directed at similar or neighboring epitopes, which may be situated within the receptor to the virus.

Animals↗
PubMed1981

Expression of retrovirus-related antigen in pregnancy. I. Antigens cross-reacting with simian retroviruses in human foetal tissues and cord blood lymphocytes.

Antisera to Mason-Pfizer or Baboon Endogenous Virus possessed complement-dependent cytotoxicity for cell lines chronically infected with these viruses, with some degree of cross-reaction. When appropriately absorbed with virus-free cells, the antisera were not cytotoxic for lymphocytes of adult males but lysed lymphocytes of neonates in about half of the 30 cord blood samples tested and were also cytotoxic for one third of 26 trophoblast suspensions prepared from healthy placentae. Detection of retrovirus-related antigens was no more frequent in trophoblast from 9 pre-eclamptic placentae. These viral antigens were also demonstrated in cultures of foetal tissues, but only after a period of culture and only when the cells were treated with 5-iododeoxyuridine. The results demonstrate that retroviruses are not only expressed in vivo in the placenta but can also be induced in cultures of foetal cells. Retrovirus-related antigens also seem to be present on foetal lymphocytes.

Animals↗
PubMed1981

Expression of retrovirus-related antigen in pregnancy. II. Cytotoxic and blocking specificities of immunoglobulins eluted from the placenta.

Immunoglobulins, mostly of the IgG class, were detected in eluates of the placenta of 75% of 50 healthy women in their first or second pregnancy, 92% of 30 women with more than two pregnancies, and 87% of 23 pre-eclamptic patients. The immunoglobulins were assayed for complement-dependent cytotoxicity on human and monkey cell-lines, as well as on the same cells chronically infected with either Mason-Pfizer Virus (M-P V) or Baboon Endogenous Virus (BeV). The frequency of cytotoxic reactions was very low, except with immunoglobulins from the pre-eclamptic placentae, where one third of the samples lysed virus-infected cells with occasional killing of virus-free cells. All placental immunoglobulins which were not cytotoxic were then assayed for blocking activity by testing whether they could compete with the action of anticellular sera of virus-free cells, or with the toxic effect of antiviral sera on virus producing cells. 64% of the immunoglobulins from normal placentae competed with antiviral antibodies while only 17% blocked the action of anticellular sera. The frequency of blocking immunoglobulins was no greater in eluates from pre-eclamptic placentae. The data indicate that the placenta possesses retrovirus antigen sites which bind blocking antibodies in normal pregnancy and complement-dependent cytotoxic antibodies in pre-eclampsia.

Animals↗