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Biomedical subjects

L Lamontagne

Publications and source records attributed to L Lamontagne.

At least 19 recordsLinked to original sources
PubMed1991

Serologic survey of white-tailed deer on Anticosti Island, Quebec for bovine herpesvirus 1, bovine viral diarrhea, and parainfluenza 3.

In 1985 unusual mortality was observed among the 3- to 4-yr-old white-tailed deer (Odocoileus virginianus) on Anticosti Island, Québec (Canada). A viral pathogen was suspected to be the cause of the deaths. Thus, a serologic survey for bovine herpesvirus 1 (BHV-1), bovine viral diarrhea (BVD) virus and parainfluenza-3 (PI-3) virus was conducted. We examined 396 deer sera from 1985. Results indicated that the high mortality mainly afflicted 3- to 4-yr-old deer. In 1985, 57% of deer sampled were seropositive for viral neutralizing antibodies against BHV-1. Prevalences decreased over the next 2 yr of the survey. Prevalence of antibodies against PI-3 virus, determined by hemagglutination inhibition test, remained high (82% to 84%) for the 3 yr period. No deer were seropositive for neutralizing antibodies against BVD virus during the survey period. Analysis of antibodies against BHV-1 and PI-3 viruses according to sex, age and antibody titers revealed that an epizootic BHV-1 infection occurred in 1985; PI-3 infection appears to be enzootic in Anticosti deer.

Age Factors↗
PubMed1990

Immune cell tropisms of attenuated MHV3 viruses isolated from brains of chronically infected mice.

Isolation of infectious viruses from the brain during a chronic neurological disease is infrequent because persistent viruses differ from the parental virus in their virulence and in the development in genomic or replication defects. We have isolated mouse hepatitis virus 3 (MHV3) variants from the brain of chronically infected mice up to 105 days postinfection by culture on overconfluent L2 cells. In spite of atrophy and leukopenia observed in lymphoid organs of these mice, no viruses were isolated in numerous attempts. In contrast, defective-interfering viruses were detected in peritoneal exudate cells from chronically-infected mice. Brain-derived viruses differ from parental virus in their delayed fusion activity and attenuated pathogenicity for C57BL/6 and A/J mice. The attenuated brain isolates have ceased to replicate in thymocytes but replicated in nonadherent spleen and peritoneal exudate cells.

Animals↗
PubMed1989

Mouse hepatitis virus 3 pathogenicity expressed by a lytic viral infection in bone marrow 14.8+ mu+ B lymphocyte subpopulations.

Mouse hepatitis virus type 3 (MHV3) provides an excellent model for studying viral-B lymphocyte interaction in the immune system, which plays an important role in the outcome of an acute disease. Bone marrow B lymphocyte subpopulations, at various times postinfection, were studied in genetically C57BL/6 and resistant A/J mice, infected with pathogenic L2-MHV3 and its nonpathogenic variant, YAC-MHV3. B lineage cell subpopulations were identified by double immunofluorescence assays using mAb of terminal deoxynucleotidyl transferase, 14.8 and cytoplasmic (cu) or surface (su) Ig mu-chains. Results revealed diminished percentage and absolute number in the bone marrow 14.8+ mu+ B lymphocyte subpopulations, including pre-B (cu+ su-) and B (cu+ su+) cells of L2-MHV3-infected susceptible C57BL/6 mice; whereas, slight or no increase was evident in the cell subpopulations of L2-MHV3 infected resistant A/J mice or in YAC-MHV3 infected in both strains of mice. Abnormal large-sized forms of the 14.8+ mu+ cells occurred, at 48-h postinfection, in L2-MHV3-infected susceptible C57BL/6 mice only. In contrast, no change in the percentage and absolute number of precursor cells (terminal deoxynucleotidyl transferase positive) and pre pre-B cells (14.8+ mu-) were detected in all infected mice. In vitro L2-MHV3 infection of C57BL/6 bone marrow purified B lineage cell subpopulations showed that pre-B (cu+ su-) and B (cu+ su+) cells became abnormally large in size and depleted in number as a result of a productive and lytic viral replication. Low L2-MHV3 viral replication occurred in these cell subpopulations of A/J mice but no YAC-MHV3 virus was produced in the cells of both strains of mice. Pre pre-B (14.8+ mu-) cells in both strains were not permissive to L2-MHV3 or YAC-MHV3 viral replication. These results are discussed with regard to the role of humoral immunodeficiency in the pathogenic process.

Acute Disease↗
PubMed1989

Mouse hepatitis virus 3 replication in T and B lymphocytes correlate with viral pathogenicity.

Viral pathogenicity may be regulated by host defense mechanisms at the virus-immune cell interaction level. The immune system plays an important role in the outcome of acute disease induced by the mouse hepatitis virus type 3 (MHV3) virus. The lymphoid cells act as effectors in the virus elimination as well as targets for viral replication. In order to demonstrate a correlation between MHV3 pathogenicity and viral replication in lymphocytes, genetically-determined resistant A/J and susceptible C57BL/6 mice were infected with pathogenic (L2-MHV3) or nonpathogenic (YAC-MHV3) viral strains. Pathogenicity and histopathologic studies have revealed that lymphoid organs such as thymus and spleen, showed injuries or atrophy in susceptible mice infected with L2-MHV3. No histopathologic lesions in the lymphoid organs occurred in C57BL/6 mice infected with YAC-MHV3 or A/J mice infected with both viruses. The mechanisms involved in the lymphoid injuries were studied regarding viral replication in the lymphoid organs and cells in infected mice. Results indicate that cell depletion in lymphoid organs is caused by a complete viral replication in lymphoid cells. Thy1.2+ and surface IgM+ lymphoid cells from susceptible C57BL/6 mice infected with L2-MHV3 were permissive to viral replication and to subsequent cell lysis. No cell lysis, however, occurred in lymphoid cells from C57BL/6 mice infected with YAC-MHV3 and A/J mice infected with both virus strains. In vitro studies, with purified T and B cell populations were performed to determine the mechanism effecting susceptibility or resistance to viral-induced cell lysis occurring in such cells. A blockade, probably occurring at the viral RNA polymerase activity level, prevents viral replication in resistant cells between the stages of fixation of the virus at the cell-surface receptor and the viral protein translation. These experiments indicate that an intrinsic virus-specific resistant mechanism occurs in lymphoid cells that plays a major role in the viral pathogenicity.

Animals↗
PubMed1989

Cystic schwannoma of the brainstem.

A rare case of cystic schwannoma occurring in the brainstem in the absence of von Recklinghausen's disease is reported. This appears to be the first case in the literature of a cystic schwannoma ever described in this location. While the exact origin of this tumor in this unusual location remains uncertain, different hypotheses are discussed and the possible origin of this tumor from perivascular elements in the brainstem is seriously considered.

Brain Neoplasms↗
PubMed1989

Host cell resistance to mouse hepatitis virus type 3 is expressed in vitro in macrophages and lymphocytes.

Phenotypic expression of in vivo sensitivity to mouse hepatitis virus type 3 (MHV3) was studied in vitro in macrophages and lymphocytes. MHV3 infections were induced in peritoneal exudate (PE), nonadherent spleen (NAS) and thymus (THY) cells from resistant A/J, susceptible C57BL/6 or semisusceptible (C57BL/6xA/J)F1 mice. Differences in cytopathic effect, cell viability and virus titers were found only at 48 hrs postinfection (p.i.). "Carrier state" infections were performed at 48 hrs p.i. by transfer of supernatants of infected cells to newly collected cells originating from the same strain of mice. A passage-dependent restriction of viral replication was detected in vitro and was expressed in PE, NAS and THY cells as a recessive phenotype. No defective-interfering viral particles were involved in the restriction of viral replication. Results obtained with crossed infections and determination of the number of productively infected cells demonstrated that restriction of viral replication in macrophages and lymphoid cells from resistant A/J mice is controlled by a genetically-determined intrinsic cellular mechanism acting principally on the level of production of infectious viral particles by the infected cell.

Animals↗
PubMed1989

Serological evidence of bovine herpesvirus 1-related virus infection in the white-tailed deer population on Anticosti Island, Quebec.

High white-tailed deer (Odocoileus virginianus) population densities and the occurrence of harsh environmental conditions are present on Anticosti Island, located in the Gulf of Saint-Lawrence (Quebec, Canada). This island is the northernmost region of white-tailed deer distribution in northeastern North America. The aim of this work was to determine whether a herpesvirus serologically related to bovine herpesvirus 1 (BHV1) may occur in a stressed white-tailed deer population. One hundred one deer sera were collected from apparently healthy animals during the hunting season from September to late November 1985. Fifty-three percent of tested deer were positive to the seroneutralization test using Colorado strain of BHV1 virus. Higher percentages of seropositivity were observed in animals of both sexes greater than 4-yr-old. Analysis of antibody titers in seropositive animals according to age suggests that BHV1-related viral infection is endemic in the Anticosti Island deer population. It is postulated that environmental stress may induce immunosuppression of certain infected and/or carrier animals in their population that shed virus for long periods of time.

Age Factors↗
PubMed1989

Modulation of the cellular immune responses to T-cell-dependent and T cell-independent antigens in lambs with induced bovine viral diarrhea virus infection.

Functional interaction between lymphoid cells and lymphotropic viruses is particularly evident for bovine viral diarrhea virus (BVDV) in cattle and its closely related virus, the border disease virus (BVDV) in sheep. The most important aspect of acute or chronic phases of BVDV or BDV infection was the host's increased susceptibility to secondary bacterial or viral infection. To study the ability of BVDV to alter the development of the cellular immune responses to concomitant inoculation with T cell-dependent and T cell-independent antigens, lambs were inoculated twice with rabbit RBC and Escherichia coli lipopolysacharide (LPS) and then were infected with a cytopathic strain of BVDV at postinoculation day 3. Leukopenia characterized by lymphopenia developed after BVDV infection. Increased [3H]thymidine incorporation was observed in resting or lectin-stimulated blood mononuclear cells in the first weeks after inoculation in BVDV-infected lambs, but was followed by decreased [3H]thymidine incorporation after the second inoculation for up to 8 weeks after initial inoculation. In contrast, transient decrease of blastogenic responses, associated with toxic effect of LPS, was detected in inoculated noninfected lambs, but was followed by stimulation of cellular immune responses. Inoculated noninfected lambs had good in vitro cellular immune response to rabbit RBC and LPS antigens, whereas lymphocytes from BVDV-infected lambs could not mount lasting cellular immune responses to antigens or BVDV. Results suggest that BVDV infection in lambs modulates the ability of lymphocytes to respond to lectins or antigenic stimuli according to the time after infection.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Characterization of a ribosomal DNA clone of Brugia malayi.

The structure of ribosomal DNA (rDNA) clone pBmr7 from microfilariae of the human parasite Brugia malayi has been examined in detail by Southern blot analysis and S-1 mapping techniques. The results demonstrate that this clone contains regions homologous to 28S, 18S and 5.8S rDNAs. A noncoding or 'spacer' region lies between the 3' end of 28S rDNA and the 5' end of 18S rDNA. An AccI-Sau3AI fragment of approximately 900 bp from this spacer region cross-hybridizes to genomic DNA fragments of different sizes from Brugia pahangi and Dirofilaria immitis. The differences observed in hybridization suggest that this rDNA fragment can be used to differentiate between various filariid species.

Animals↗
PubMed1986

Identification of two subtypes of HLA-DR2 by Southern blot analysis.

We studied the polymorphism of HLA-DR2 by Southern blot analysis. Genomic DNA from 12 DR2 positive unrelated individuals was digested separately with five restriction endonucleases, Bam HI, Eco RI, Eco RV, Hind III and Pvu II. Hybridizing restriction fragments were visualized using radiolabeled beta-chain cDNA probes homologous to the DR and DQ subregions of the HLA. The results in the present study demonstrate that the two subtypes of DR2, DR2.1 and DR2.2, as defined by serological and cellular (PLT) techniques can be identified by Southern blot analysis. These two subtypes were identifiable after cleaving genomic DNA with Bam HI and EcoRV. DR2.1 correlated with restriction endonuclease fragments at 2.8 kb (DR beta) and 6.6 kb (DQ beta) after Bam HI digest, while DR2.2 correlated with a 2.9 kb (DR beta) and a 2.6 kb (DQ beta) restriction fragment after Eco RV digest. In addition, inheritance of the restriction fragment lengths defining DR2.1 and DR2.2 were observed in two families. In contrast, no differences between DR2.1 and DR2.2 were observed with the restriction enzymes Eco RI, Hind III and Pvu II.

DNA Restriction Enzymes↗
PubMed1985

Acute phase response in infectious disease.

In considering the pathology associated with infectious diseases, the most common host response to such infection is inflammation. The mechanism(s) whereby inflammation is initiated and the cell types involved will dictate the kinds of acute phase plasma changes that can be seen associated with the infection. Bacteria seem to initiate the classical type of inflammatory response and plasma protein changes similar to those seen in experimental inflammation induced by chemical means. Viruses, on the other hand, in the absence of cytopathology do not appear to induce the same kind of inflammatory changes and avoid the induction of the acute phase protein response since they may not initiate activation of monocytes and/or macrophages. Those viruses that do cause macrophage activation would be expected to have acute phase protein changes associated with that activation. Parasites, however, appear to initiate the acute phase plasma response only when their migration leads to tissue destruction and local inflammation such as caused by parasitemia with Trypanosoma cruzi in the mouse or with migration of Nippostrongylus brasiliensis in the rodent. Human parasitic diseases require much more investigation in order to clarify the role played by acute phase proteins in the subsequent establishment of the host-parasite relationship. We postulate that the macrophage or monocyte on interaction with the infectious pathogen becomes activated and secretes a number of factors, including interleukin 1 and hepatocyte-stimulating factor, which have a marked effect on the total acute phase reaction. In addition to an effect on phagocytic and immune systems, the mediators cause hepatocytes to markedly increase the secretion of plasma acute phase proteins. Some of these proteins return to the site of inflammation and interact with the infectious pathogen and/or cells and proteins of the host, thereby affecting the final outcome of inflammation. We also propose that the initial interaction of an organism such as a parasite and the mammalian host involves early recognition by the macrophage, thereby initiating both the humoral and cellular acute phase reactions and subsequently affects the immune response against the parasite. Variations in the acute phase reaction may help to explain differences in susceptibility to infectious organisms and the presence or lack of host killing mechanisms for the parasite.

Acute-Phase Proteins↗