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Biomedical subjects

D Portetelle

Publications and source records attributed to D Portetelle.

At least 109 records · Page 6Linked to original sources
PubMed1989

Infection of rats with bovine leukaemia virus: establishment of a virus-producing rat cell line.

Adult rats were infected with bovine leukaemia virus (BLV). Inoculated rats persistently produced antibodies directed against viral structural proteins. No major pathogenesis in infected rats was found during 2 years of observation. It was possible to recover the virus from rat spleen several months after infection. A cell line, R(BLV), was established from rat spleen; this contained integrated BLV provirus. R(BLV) cells kept for over 80 passages in vitro produced viral particles with the properties of BLV. Provirus reintegration and/or amplification occurred in R(BLV) cells. The cell line was found to be tumorigenic in rats, and the virus produced was immunogenic. R(BLV) cells represent the first described BLV-producing rat cell line. Proven persistent infection with BLV indirectly suggests that rats can serve as a reservoir of BLV in nature.

Animals↗
PubMed1988

The neurotrophic factor neuroleukin is 90% homologous with phosphohexose isomerase.

Neuroleukin (NLK) is a protein of relative molecular mass (Mr) 56,000 (56K) secreted by denervated rat muscle and found in large amounts in muscle, brain, heart and kidneys. The protein is a neurotrophic factor for spinal and sensory neurons and a lymphokine product of lectin-stimulated T-cells. It also induces immunoglobulin secretion by human mononuclear cells. Molecular clones of NLK have been expressed in monkey COS cells and the product was shown to have the same biological and biochemical properties as the extracted protein. NLK is abundant in muscle, brain and kidney, but is active at concentrations of 10(-9) to 10(-11) M, similar to those for other polypeptide factors. We have cloned the gene for pig muscle phosphohexose isomerase (PHI) (EC 5.3.1.9) which catalyses the conversion of glucose-6-phosphate to fructose-6-phosphate, an obligatory step in glycolysis, and determined its amino-acid sequence. Surprisingly, it is 90% homologous to the sequence of mouse neuroleukin.

Amino Acid Sequence↗
PubMed1988

Effects of an anabolic treatment before puberty with trenbolone acetate-oestradiol or oestradiol alone on growth rate, testicular development and luteinizing hormone and testosterone plasma concentrations.

Scrotal circumference, growth and hormonal status after prepubertal anabolic treatments were studied in 18 conventional Belgian White Blue bulls from 3 to 13 mo of age. Young bulls were assigned into three groups: six untreated (control) bulls, six bulls implanted with 140 mg trenbolone acetate + 20 mg oestradiol (Revalor; TBA-E2) and six bulls treated with 45 mg oestradiol (Compudose; E2). Mean scrotal circumference was similar in the three groups at Day O (between 13.0 +/- 0.3 cm to 13.4 +/- 0.7 cm). From Days O to 230, scrotal circumference was strongly inhibited in implanted bulls, 23.2 +/- 1.4, 21.7 +/- 1.0 cm, respectively, for TBA-E2 and E2 at Day 210, as compared with 29.5 +/- 2.2 cm in control bulls (P < 0.001). Afterwards, differences lessened gradually and no significant divergence was observed between the three groups from Day 310. Average plasma luteinizing hormone (LH) concentrations were similar in the three groups throughout the assay. Mean testosterone levels remained extremely low upto Day 150 in TBA-E2 and E2 groups (0.6 +/- 0.6, 1.2 +/- 0.7 ng/ml, respectively) before they increased abruptly and reached values observed in control bulls at Day 180 (4.0 +/- 1.9 ng/ml). The pulsatil character of LH and testosterone profiles was abolished by the anabolic treatments. Luteinizing hormone-releasing hormone (LHRH) injection was followed by an immediate and sharp increase in plasma LH concentrations in all groups at Day 0. Anabolic treatments strongly reduced LH and testosterone responses to LHRH in treated groups.

Journal Article↗
PubMed1988

Detection of B and T cells, with lectins or antibodies, in healthy and bovine leukemia virus-infected cattle.

Lectins, polyclonal antibodies and monoclonal antibodies (MAbs) were evaluated as markers for bovine lymphocytes obtained from healthy animals and from cattle infected with bovine leukemia virus (BLV). In the blood from healthy cattle the proportion of cells identified as T lymphocytes with the lectin Helix pomatia (HP) (67.8 +/- 6.2%) using the indirect immunofluorescence technique was similar to the proportion of cells identified by the MAbs P5 (66.1 +/- 3.8%) and BLT-1 (59.8 +/- 7.1%). The proportion of B cells in blood from healthy animals identified with a polyclonal antibody to bovine IgM (18.0%) was similar to that identified with a MAb to bovine IgM (16.2%). However, greater variation between individual values was detected with the MAb (SD = 8.2) than with the polyclonal antibody (SD = 4.0). In the blood from BLV-infected cattle with persistent lymphocytosis, both the polyclonal and the MAb revealed a threefold increase of B cells. A proportion of the B cells had an increased amount of immunoglobulin molecules in their plasma membrane as indicated by flow cytometry. The proportion of T lymphocytes, identified by the MAb P5, was reduced to one-third of that in non-infected cattle. The indirect HP labelling gave inconsistent results and seems not to detect solely T lymphocytes among blood lymphocytes from BLV-infected cattle.

Animals↗
PubMed1988

Bovine leukaemia: facts and hypotheses derived from the study of an infectious cancer.

Bovine leukaemia virus (BLV) is the etiological agent of chronic lymphatic leukaemia/lymphoma in cows, sheep and goats. Infection without neoplastic transformation was also obtained in pigs, rhesus monkeys, chimpanzees, rabbits and observed in capybaras and water-buffaloes. Structurally and functionally, BLV is a relative of human T lymphotropic viruses 1 and 2 (HTLV-I and HTLV-II) In humans, HTLV-I induces a T-cell leukaemia and its type 2 counterpart has been found in dermatopathic lymphadenopathy, hairy T-cell leukaemia and prolymphocytic leukaemia cases. At variance with HTLV-I, BLV has not been associated with neurological diseases of the degenerative type. Bovine leukaemia virus, HTLV-I and HTLV-II show clearcut sequence homologies. The pathology of the BLV-induced disease, most notably the absence of chronic viraemia, a long latency period and lack of preferred proviral integration sites in tumours, is similar to that of adult T-cell leukaemia/lymphoma induced by HTLV-I. The most striking feature of these three naturally transmitted leukaemia viruses is the X region located between the env gene and the long terminal repeat (LTR) sequence. The X region contains several overlapping long open reading frames. One of them, designated XBL-I, encodes a trans-activator function capable of increasing the level of gene expression directed by BLV-LTR and most probably is involved in "genetic instability" of BLV-infected cells of the B cell lineage. The "genetic instability" renders the infected cell susceptible to move, along a number of stages, towards full malignancy. Little is known about these events and their causes; we present some theoretical possibilities. Bovine leukaemia virus infection has a worldwide distribution. In temperate climates, the virus spreads mostly via iatrogenic transfer of infected lymphocytes. In warm climates and in areas heavily populated by haematophagous insects, there are indications of insect-borne propagation of the virus.

Animals↗
PubMed1988

Bovine leukemia: facts and hypotheses derived from the study of an infectious cancer.

Bovine leukemia virus is the etiological agent of a chronic lymphatic leukemia/lymphoma in cows, sheep, and goats. Infection without neoplastic transformation also was obtained in pigs, rhesus monkeys, chimpanzees, and rabbits, and was observed in capybaras and water buffaloes. Structurally and functionally, BLV is a relative of the human T lymphotropic viruses (HTLV-I and HTLV-II). HTLV-I induces in humans a T cell leukemia, and its type II counterpart has been found in dermatopathic lymphadenopathy, hairy T cell leukemia and prolymphocytic leukemia cases. At variance with HTLV-I, BLV has not been associated with neurological diseases of the degenerative type. BLV, HTLV-I, and HTLV-II show clearcut sequence homologies. The pathology of the BLV-induced disease, most notably, the absence of chronic viremia, a long latency period, and a lack of preferred proviral integration sites in tumors, is similar to that of adult T cell leukemia/lymphoma induced by HTLV-I. The most striking feature of the three naturally transmitted leukemia viruses is the X region located between the env gene and the LTR sequence. The X region contains several overlapping long open reading frames. One of them designated XBL-I encodes a trans-activator function capable of increasing the level of gene expression directed by BLV-LTR and most probably involved in "genetic instability" of BLV-infected cells of the B cell lineage. The genetic instability puts the cell into a context of fragility and ready to move along a number of stages towards full malignancy. Little is known about these events and their causes; we have presented some theoretical possibilities. BLV infection has a worldwide distribution. In temperate climates the virus spreads mostly via iatrogenic transfer of infected lymphocytes. In warm climates and in areas heavily populated by hematophageous insects, there are indications of insect-born propagation of the virus.

Animals↗
PubMed1988

Even transcriptionally competent proviruses are silent in bovine leukemia virus-induced sheep tumor cells.

To investigate the role of proviral integration and expression in cellular transformation induced by bovine leukemia virus (BLV), three BLV-induced tumors harboring a single proviral copy were selected upon restriction and hybridization analysis. Tumors 344 and 395 were shown to contain a full-size proviral copy, whereas in tumor 1345 the provirus appeared to be heavily deleted. RNA gel blot hybridization with an antisense RNA probe showed no transcription of the viral sequences in the fresh tumors or in sheep tumor cells growing in vitro. The proviruses were cloned and transfected in mammalian cell lines. Transient-expression experiments revealed that the complete proviruses were still able to express the trans-activating protein (Tat) as well as structural proteins, demonstrating that the nonexpression of a provirus in a tumor cell does not necessarily imply a structural alteration of the viral information. In contrast, sequence analysis of the provirus with a large deletion and transient-expression assays proved that this truncated provirus, isolated from a tumor, was unable to code for viral proteins. These data indicate that expression of viral genes, including tat, is not required for the maintenance of the transformed state.

Animals↗
PubMed1988

Experimental transmission of enzootic bovine leukosis to sheep: latency period of the tumoral disease.

In the field of viral oncogenesis the latency period is the interval between detectable establishment of infection and appearance of a tumor. Between 1969 and 1985, a total of 60 sheep died with lymphosarcoma. They were inoculated with BLV-positive blood from various donor cows, by various routes, at various ages, etc. A statistical analysis was performed trying to find a correlation between the length of the latency period and, on the other hand, one or more factors, such as sex, family lineage, identity of the dam, age at inoculation, route of inoculation, or origin of the inoculum. None of the above mentioned parameters has a significant effect on the length of the latency period. In two series of sheep inoculated with decreasing number of lymphocytes from BLV-positive donor cows, hematological disorders and tumors appeared at first in recipient animals inoculated with the higher doses of infectious blood. Thus, the inoculated dose has an effect upon the length of the latency period; the higher the dose inoculated, the shorter the latency period. This finding suggests an explanation to the natural occurrence of multiple case herds as opposed to no-tumor case herds. A multiple case herd fulfills two conditions: the presence of a good donor and an efficient route of transmission allowing the transfer to the recipient of the optimal amount of infected blood.

Animals↗
PubMed1987

Expression of a cDNA clone corresponding to the long open reading frame (XBL-I) of the bovine leukemia virus.

Nucleotide sequence analysis of a cDNA clone corresponding to the XBL-I open reading-frame of bovine leukemia virus (BLV) revealed that the AUG initiation codon was located 44 bases downstream from that of the env gene and was part of the p34x mRNA splice donor. . .ATGG/GTAA at the end of the pol gene sequence. RNA from this clone was synthesized in vitro by the SP6 RNA polymerase and translated into a 34,000 mol wt protein in rabbit reticulocyte lysates. The protein (p34x) is recognized in Western blots by most sera of BLV-infected sheep and tumor-bearing cattle, by an anti-synthetic peptide rabbit serum, and by the serum of a rabbit immunized by XBL-I RNA programmed reticulocyte lysates. Both sera react with a 34,000 mol wt protein present in nuclei of BLV-infected cells.

Base Sequence↗
PubMed1987

Experimental transmission of enzootic bovine leukosis to cattle, sheep and goats: infectious doses of blood and incubation period of the disease.

A group of 49 BLV-free recipient animals (24 cattle, 15 sheep and 10 goats) were inoculated intradermally with serial dilutions of blood collected on two BLV-positive donor cows. One donor had a high lymphocytosis and high antibody titers to gpBLV antigens; these two parameters were low for the second donor. The number of lymphocytes which induced BLV infection in recipient animals varied widely with the donor. The high infectivity of a donor seemed to be correlated with high lymphocytosis and high antibody titers to gpBLV antigens. Identification and removal of infectious animals would reduce or stop the spread of the infection in a herd, and could be used in the strategy to eradicate the disease. A given inoculum can be infectious in sheep and, at the same time, harmless in cattle. The incubation periods, apparently shorter in sheep, were generally in the range from 2 to 5 weeks for the three species, and exceptionally above.

Animals↗
PubMed1987

Provirus integration of bovine leukemia virus into DNA of infected human myeloma cells.

Sixty clones of bovine leukemia virus-infected B-human myeloma ARH77 cells were isolated. The DNAs of all clones were examined for BLV provirus integration by Southern blotting analysis. Proviral sequences were found in DNAs of two clones. One of them (clone I B3) contained one proviral copy with a deletion of approximately 5.5 kb; the other one (clone I F9) carried three integrated proviruses. Viral proteins of 70,000, 42,000 and 35,000 M. W. were found in extracts of clone I F9. In clone I B3 only the 70,000 M.W. protein was detected.

Cell Line↗
PubMed1987

Bovine leukaemia: facts and hypotheses derived from the study of an infectious cancer.

Bovine leukaemia virus (BLV) is the aetiological agent of a chronic lymphatic leukaemia/lymphoma in cows, sheep and goats. Infection without neoplastic transformation has also been demonstrated in pigs, rhesus monkeys, chimpanzees and rabbits and observed in capybaras and water buffaloes. Structurally and functionally, BLV is a relative of human T lymphotropic viruses 1 and 2 (HTLV-I and HTLV-II) since all three viruses show clear-cut sequence homologies. The pathology of the BLV-induced disease, most notably the absence of chronic viraemia, a long latency period and lack of preferred proviral integration sites in tumours, is similar to that of adult T-cell leukaemia/lymphoma induced by HTLV-I. The most striking feature of the three naturally transmitted leukaemia viruses is the X region located between the env gene and the long terminal repeat (LTR) sequence. The X region contains several overlapping long open reading frames, one of which, designated XBL-1, encodes a trans-activator function capable of increasing the level of gene expression directed by BLV-LTR and is most probably involved in genetic instability of BLV-infected cells of the B-cell lineage. The 'genetic instability' may put the cell into a state of fragility, ready to move along a number of stages towards full malignancy. Little is known about these events and their causes and we present some theoretical possibilities. BLV infection has a worldwide distribution. In temperate climates the virus spreads mostly through iatrogenic transfer of infected lymphocytes. In warm climates and in areas heavily populated by haematophagous insects, there are indications of insect-borne propagation of the virus.

Animals↗
PubMed1986

Replicative and cytopathic potential of HTLV-III/LAV with sor gene deletions.

The genome of the human T-lymphotropic virus type III (HTLV-III/LAV) has the potential to encode at least three polypeptides in addition to those encoded by the gag, pol, and env genes. In this study, the product of the sor (short open reading frame) region, which overlaps the 3' end of the pol gene, was found to be a protein with a molecular weight of 23,000. An assay was developed for testing the ability of cloned HTLV-III proviruses to produce viruses cytopathic for T4+ lymphocytes. In the cell line used, C8166, neither the HTLV-III sor gene product nor the complete 3'-orf gene product were necessary for the replication or cytopathic effects of the HTLV-III.

Cell Line↗
PubMed1986

Monoclonal antibodies to hemagglutinin-neuraminidase and fusion glycoproteins of Newcastle disease virus: relationship between glycosylation and reactivity.

Eighteen hybridoma lines obtained by immunization of mice with Newcastle disease virus (NDV) lentogenic strain La Sota or velogenic strain Italien produced hemagglutinating monoclonal antibodies. The 18 monoclones were divided into four groups according to their reactivity toward native hemagglutinin neuraminidase protein (HN), nonglycosylated HN precursor, and heat-denatured HN blotted on nitrocellulose membranes. Only group II reagents were reactive toward their targets in all conditions tested. They were considered sequence-specific antibodies. Group I antibodies did not require glycosylation but lacked reactivity towards the denatured glycosylated antigen. Monoclonal antibodies from group III recognized only the native HN. Group IV was made up of a single monoclone that lacked reactivity with NDV Italien but recognized the La Sota strain in hemagglutination inhibition and enzyme-linked immunosorbent assays. Five hybridoma lines produced monoclonal antibodies which neutralized viral infectivity but failed to inhibit hemagglutination. One monoclonal antibody obtained after immunization of mice with NDV La Sota showed a low neutralization index versus NDV Italien. Four monoclonal antibodies derived from mice immunized with NDV Italien showed higher neutralization indices towards this strain. Neither the denatured F protein nor its nonglycosylated precursor was reacted against by the five monoclonal antibodies.

Animals↗
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

The diagnosis of enzootic bovine leukosis.

This paper reviews the clinical and virological diagnostic procedures for enzootic bovine leukosis (EBL). The clinical diagnosis must be always confirmed by a specific laboratory test for Bovine Leukaemia Virus (BLV). Many virological tests were proposed. The sensitivity of all the diagnostic methods is sufficient to do an early detection of a BLV infection on an individual base. Advantages of the highly sensitive methods like RIA and ELISA appear when the samples to be tested have naturally very low antibody titers (individual milk, bulk milk, pooled sera).

Animals↗