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Y Riviere

Publications and source records attributed to Y Riviere.

At least 19 recordsLinked to original sources
PubMed2005

Wastewater stabilisation ponds: Sludge accumulation, technical and financial study on desludging and sludge disposal case studies in France.

Waste stabilisation pond treatment was widely developed during the 1980s in France, where there are now over 3,000 plants. Desludging the ponds has now become essential. In 19 primary facultative ponds, in operation for 12-24 years, the net average sludge accumulation rate was 19 mm/yr. The average per capita accumulation rates ranged from 0.04-0.148 m3/person.year (mean of 0.08 m3/person.year). In primary facultative ponds the volume of sludge represented 15-39% of the total volume of the basin. A filling rate above 30% necessitates desludging. In France, a desludging interval of 15 years is recommended for primary facultative ponds. The cost evaluation of desludging and landspreading showed differences according to the desludging technique used. Desludging after emptying the water had an average cost of 38 Euro/m3 of sludge with 10% dry solid (range from 20 to 83 Euro/m3). Under-water desludging was 50% more expensive. Although desludging is carried out only after several years of operation, its cost must be allowed for in the annual operation and maintenance costs of the process. It can be estimated to be 3 ł/person.year. Even with this additional cost, waste stabilisation pond treatment remains less expensive than other treatment processes.

France↗
PubMed1997

Potential deleterious effect of anti-viral cytotoxic lymphocyte through the CD95 (FAS/APO-1)-mediated pathway during chronic HIV infection.

The potential deleterious effect through a CD95-based pathway of anti-viral cytotoxic lymphocyte (CTL) during HIV-infection was studied. The present paper reports that a Nef specific CTL line derived from an HIV-infected person is able to kill not only Nef-expressing target cells but also CD95+ compliant Jurkat cells. The two mechanisms of cytotoxicity, i.e. perforin-vs-CD95-dependent were differentiated according to their respective Ca(2+)-dependence. The existence of the dual killing machinery in the anti-HIV CTL line was correlated with the coexpression in these cells of perforin and CD95-L molecules. A model of AIDS pathogenesis involving the deleterious effect through the CD95 pathway of the viral specific CTL response is discussed.

Antigen-Presenting Cells↗
PubMed1995

Sequence constraints and recognition by CTL of an HLA-B27-restricted HIV-1 gag epitope.

Previous studies on the variation of an immunodominant HLA-B27-restricted HIV-1 gag p24 epitope (KRWIIL GLNK, amino acids 263-272) have demonstrated the persistence of variants recognized by CTL. Sequence comparisons of HIV isolates showed that this region is relatively conserved and as a consequence might restrict antigenic variation. To evaluate the possibility of HIV-1 to yield infectious mutants of this epitope that lack the ability to bind to HLA-B27 or escape HLA-B27-restricted CTL recognition, single-point mutations were constructed in the infectious molecular clone of HIV-1 Lai. Changes of arginine 264, the anchor amino acid for HLA-B27, to lysine or glycine resulted in infectious HIV-1 variants. The respective synthetic peptides showed reduced ability to sensitize target cells for CTL recognition and a corresponding loss of binding affinity to HLA-B27. In contrast, mutation of glycine 269 to lysine or glutamate abrogated HIV-1 infectivity. The corresponding peptides were able to bind to HLA-B27 but were not recognized by CTL. These data show that HIV-1 tolerates some genetic variation of the HLA-B27-restricted CTL epitope in gag p24 and that single-point mutations can alter quantitatively the immunologic properties. Further, it demonstrates that the mere nonrecognition of peptides derived from quasispecies analysis of small regions might simply correspond to nonviable virus variants and cannot be taken as evidence for CTL escape mutants. Together with the previously published data on the persistence of CTL epitopes, these results suggest that CTL do not play a major role in driving HIV-1 evolution in vivo.

Amino Acid Sequence↗
PubMed1990

T- and B-lymphocyte responses to human immunodeficiency virus (HIV) type 1 in macaques immunized with hybrid HIV/hepatitis B surface antigen particles.

Recombinant human immunodeficiency virus (HIV)/hepatitis B surface antigen (HBsAg) subviral particles of dual antigenicity and immunogenicity were obtained by fusing 84 amino acids of the HIV type 1 external envelope glycoprotein within the pre-S2 part of the hepatitis B middle protein (M.-L. Michel, M. Mancini, E. Sobczak, V. Favier, D. Guétard, E.-M. Bahraoui, and P. Tiollais, Proc. Natl. Acad. Sci. USA 85:7957-7961, 1988). We now describe the humoral and cellular immune response of rhesus monkeys immunized with these hybrid particles. Macaque antisera raised by subcutaneous injections of the HIV/HBsAg particles were shown to be specific for HIV in peptide-binding assays. Moreover, we were able to generate in these vaccinated animals a T-cell-proliferative response to both parts of the hybrid particle, i.e., HIV and HBsAg. These results establish the presence of a T-cell epitope in this HIV segment, which has been shown previously (L.A. Lasky, G. Nakamura, D. H. Smith, C. Fennie, C. Shimasaki, E. Patzer, P. Berman, T. Gregory, and D. J. Capon, Cell 50:975-985, 1987) to be an important domain involved in the binding of the virus to its cellular receptor, the CD4 molecule. This work demonstrates the feasibility of using the HBsAg subviral particle as a carrier protein for the presentation of foreign immunogenic epitopes to the immune system.

Animals↗
PubMed1989

Cell-mediated immune proliferative responses to HIV-1 of chimpanzees vaccinated with different vaccinia recombinant viruses.

The only animal that can be reproducibly infected with HIV, and that thus provides an experimental system for testing the effectiveness of prototype vaccines, is the chimpanzee. We compared proliferative responses to HIV and to vaccinia virus (VV) antigens of lymphocytes taken at various times from chimpanzees vaccinated with recombinant VV expressing different HIV genes. Animals were immunized with the original VV strain, as control, or with constructs expressing gp160 (VV160) given exclusively or in combination with one or two other constructs producing p25 (VV25), F/3'-orf (VVF), or the human interleukin-2 (IL-2) gene, which was included in an attempt to amplify immune responses. Irrespective of the HIV gene utilized, lymphocyte proliferation to HIV was usually weak and rapidly decreased after each inoculation, contrasting with strong and sustained responses to VV. Lack of adequate recall reactivity after challenge with fixed autologous lymphocytes expressing VV-produced HIV antigens indicated that vaccination resulted only in low levels of HIV-specific memory cell priming. The use of IL-2-producing VV did not lead to increased responsiveness. Reactivity to soluble purified gp160, but not to p25, could be detected in PBL from animals that had received both VV160 and VV25, while immunization with VVF resulted in a significant response to this protein in one of two animals. The transient nature of T cell reactivity to HIV might explain why, in similar studies, chimpanzees were not protected from infection with live HIV.

Animals↗
PubMed1989

Human immunodeficiency virus-specific cytotoxic responses of seropositive individuals: distinct types of effector cells mediate killing of targets expressing gag and env proteins.

By using target cells that expressed isolated env, gag, p27nef, or p23vif molecules introduced by recombinant vaccinia viruses containing genes encoding these polypeptides, it was possible to identify env, gag, p27nef, and p23vif as cytolytic target antigens for freshly isolated blood cells from human immunodeficiency virus 1 (HIV-1) seropositive patients. Most of the patients tested (95%) manifested a specific cytotoxic activity against vaccinia virus-env-infected target cells. The env-specific cytotoxic activity was not restricted by the major histocompatibility complex and was not mediated by T lymphocytes, as shown by the absence of blocking effect with an anti-CD3 monoclonal antibody and by the inefficiency of CD3+, CD8+, or CD4+ and CD8+ depletion to reduce the cytotoxic activity against the env-expressing target cells. In the same conditions, the cytotoxic activity specific for gag was abrogated and gag major histocompatibility complex-restricted cytotoxic T lymphocytes were detected in 85% of the subjects tested. Therefore, in a HIV-1 seropositive subject, distinct types of effector cells mediate the lysis of target cells expressing gag and env proteins.

Antibodies, Monoclonal↗
PubMed1988

Loss of CD4 membrane expression and CD4 mRNA during acute human immunodeficiency virus replication.

Using mAbs and genomic probe to the CD4 molecule, the HIV receptor, we demonstrated that HIV replication induces the disappearance of its functional receptor from the cell surface by two distinct mechanisms. First, after being expressed onto the cell surface, HIV envelope gp110 will complex CD4, efficiently masking the CD4 epitope used by the virus to bind its receptor. This phenomenon occurs on the surface of each infected cell and is not due to the release of soluble gp110; infection with recombinant HIV/vaccinia viruses expressing a mutated HIV env gene designed to prevent gp110 release from the cell surface induces a similar gp/CD4 complexes formation. Second, virus replication induces a dramatic and rapid loss of CD4 mRNA transcripts, preventing new CD4 molecules from being synthesized. These two mechanisms of receptor modulation could have been developed to avoid reinfection of cells replicating the virus as well as to produce more infectious particles. These results suggest that the classical virus interference documented for other retroviruses might not only be due to receptor/envelope interaction, but might also depend on receptor gene expression.

Cell Membrane↗
PubMed1987

Molecular characterization of the genomic S RNA segment from lymphocytic choriomeningitis virus.

We have used cDNA clones derived from the genomic S RNA segment of lymphocytic choriomeningitis virus (LCMV), Armstrong strain, as hybridization probes to monitor virus gene expression during acute infections. Our results with strand-specific probes confirm the ambisense character of the LCMV S RNA segment and document the presence of both genomic sense and genomic complementary sense RNA species over the time course of infection. We have used nucleotide sequence information to predict primary amino acid sequences for the major viral structural proteins, nucleoprotein (NP) and glycoprotein (GP-C). Antibodies raised against synthetic peptides derived from these predicted protein sequences have indicated that the gene order for the S segment is 3' NP----5' GP-C and provided direct demonstration that the GP-1 portion of the GP-C precursor is encoded nearest the 5' end of the S segment. Comparison of the predicted amino acid sequences for NP and GP-C between the Armstrong CA-1371 strain and the WE strain shows over 90% amino acid identity. This suggests that significant differences described for the pathogenic potential of the Arm and WE strains in C3H mice reside in one or a very few critical amino acid changes.

Amino Acid Sequence↗
PubMed1987

Perturbation of differentiated functions in vivo during persistent viral infection. III. Decreased growth hormone mRNA.

Lymphocytic choriomeningitis virus (LCMV) persistent infection that results from the inoculation of C3H/St newborn mice causes growth hormone (GH) deficiency and associated disease characterized by both reduced weight and serum glucose levels. Molecular analysis of pituitary nucleic acids shows GH deficient mice have, on average, fivefold reduced levels of GH mRNA although the histopathology of such GH producing cells is normal. Northern blots indicate that the length of GH mRNA is comparable in the GH deficient, virus infected mice and the GH normal, uninfected age-matched controls. Hence, truncated GH mRNA cannot account for hormonal defect. Mice infected congenitally through mating of persistently infected parents have normal growth and blood glucose levels. GH mRNA levels in pituitaries of these mice are equivalent to those of uninfected age-matched controls but significantly greater than those seen in neonatally infected GH deficient mice. Although infectious virus titers in the sera are equivalent in congenitally and neonatally infected age- and sex-matched mice, virus titers are significantly lower in pituitaries and brains of the congenitally infected mice when compared to neonatally inoculated mice. Additionally, the number of GH-producing pituitary cells expressing viral proteins is less in congenitally infected mice relative to those in neonatally inoculated mice. Hence there is a direct association between viral replication in GH-producing cells, lowered GH mRNA, and GH deficiency.

Animals↗
PubMed1986

Genetic reassortants of lymphocytic choriomeningitis virus: unexpected disease and mechanism of pathogenesis.

Reassortant viruses of different strains of lymphocytic choriomeningitis viruses cause lethal disease after inoculation into neonatal BALB/c WEHI mice, but, in contrast, parental strains or reciprocal reassortants do not cause lethal disease. The disease is characterized by inhibition of growth and death. The pathogenic mechanism is the induction of interferon combined with higher virus titers and subsequent liver necrosis. The generation of lethal reassortants from nonlethal parent viruses likely has implications for understanding the outbreaks of unanticipated virulent disease within a viral family.

Animals↗
PubMed1986

Biology of cloned cytotoxic T lymphocytes specific for lymphocytic choriomeningitis virus. V. Recognition is restricted to gene products encoded by the viral S RNA segment.

Lymphocytic choriomeningitis virus (LCMV) Armstrong (ARM) strain-specific, H-2d-restricted CTL effectively lyse syngeneic targets infected by LCMV ARM, but show reduced killing of LCMV Pasteur (PAST) strain-infected H-2d cells. We have reassorted the two RNA segments, large (L) and small (S), of LCMV ARM and PAST to generate LCMV with genotypes of L ARM/S PAST and L PAST/S ARM. By using these reassortants and both LCMV primary CTL and CTL clones, we report that the induction, recognition, and lysis of LCMV-specific CTL depend on the S RNA segment and the genes it encodes.

Animals↗
PubMed1985

Perturbation of differentiated functions during viral infection in vivo. II. Viral reassortants map growth hormone defect to the S RNA of the lymphocytic choriomeningitis virus genome.

Lymphocytic choriomeningitis virus (LCMV) Armstrong caused disordered growth and glucose metabolism secondary to growth hormone deficiency in infected C3H/St mice. In contrast, LCMV strain WE replicated in fewer growth hormone-producing cells, failed to disrupt growth hormone synthesis, and did not cause growth hormone-induced disease in infected, matched controls. The generation of genetic reassortant viruses between the virulent strain of LCMV:Armstrong and the avirulent strain, LCMV:WE, is reported. Using such reassortants and both parental strains of virus in C3H/St mice, the perturbation of growth hormone synthesis was clearly mapped to the S RNA segment of LCMV:ARM.

Animals↗
PubMed1985

Enhancement of natural killer cell activity and 2-5A synthetase in operable breast cancer patients treated with polyadenylic; polyuridylic acid.

Treatment of operable breast cancer patients with a single injection of 60 mg poly(A); poly(U) (polyadenylic, polyuridylic acid) resulted in an enhancement of natural killer (NK) cell cytotoxicity against human myeloid K562 target cells. Furthermore, the level of 2-5A synthetase in peripheral blood lymphocytes of such patients was increased after the treatment. Both of these effects, measured 24 and 48 hours after the injection of poly(A); poly(U), were statistically significant compared to their respective levels before the treatment. These events, therefore, may be used as markers to monitor the immediate response of patients toward treatment with this synthetic double-stranded RNA.

2',5'-Oligoadenylate Synthetase↗
PubMed1985

Comparison of the effects of rabies virus infection and of combined interferon and poly(I).poly(C) treatment on the levels of 2',5'-adenyladenosine oligonucleotides in different organs of mice.

Intracellular levels of 2',5'-adenyladenosine oligonucleotides were analyzed in different organs of mice during the course of a rabies virus infection. Phosphorylated and nonphosphorylated 2',5'-adenyladenosine oligonucleotides were measured by radioimmunoassay and analyzed further by HPLC. As the infection progressed, concentrations of phosphorylated 2',5'-adenyladenosine oligonucleotides increased strongly, reaching their maxima late in the infection. In contrast, concentrations of the nonphosphorylated 2',5'-adenyladenosine oligonucleotides decreased. A similar phenomenon was observed in spleens analyzed at intervals after treatment of noninfected mice with interferon and poly(I).poly(C) and to a lesser extent after treatment of noninfected mice with interferon and poly(I).poly(C) and to a lesser extent after treatment with poly(I).poly(C) alone, but not after treatment with interferon alone. The products which accumulated during virus infection were primarily phosphorylated dimers whereas during combined interferon and poly(I).poly(C) treatment, the entire range of phosphorylated molecules from dimer to pentamer was present. These data show that infection of mice with rabies virus provokes both the induction and the activation of 2-5A synthetase, as does interferon and poly(I).poly(C) treatment. However, our data indicate that the intracellular products are different in the two situations: the species active on the nuclease were only detected in interferon- and poly(I).poly(C)-treated mice. The absence of molecules able to activate the 2-5A-dependent nuclease in virus-infected mice might well be one of the reasons why the interferon system is ineffective in rabies virus infection.

Adenine Nucleotides↗