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L Lamontagne

Publications and source records attributed to L Lamontagne.

At least 19 recordsLinked to original sources
PubMed2004

Murine viral hepatitis involves NK cell depletion associated with virus-induced apoptosis.

Mouse hepatitis virus type 3 (MHV3), a coronavirus, is an excellent animal model for the study of immunological disorders related to acute and chronic hepatitis. In this study, we have verified if the fulminant hepatitis induced by MHV3 could be related to an impairment of innate immunity. Groups of three C57BL/6 mice were infected with the pathogenic L2-MHV3 or attenuated YAC-MHV3 viruses, and the natural killer (NK) cell populations from liver, spleen and bone marrow were analysed. The percentage of intrahepatic NK1.1(+)T cell receptor (TCR)- cells did not increase while NK1.1(+)TCR(inter) cells decreased in both L2-MHV3- and YAC-MHV3-infected mice. Concurrently, splenic and myeloid NK1.1+ cells decreased in L2-MHV3-infected mice. However, the cytotoxic activity of NK cells increased in liver and decreased in bone marrow from pathogenic L2-MHV3-infected mice while no modification was detected in YAC-MHV3-infected mice. Flow cytometric analysis revealed that both normal and larger splenic or myeloid NK cells decreased more in pathogenic L2-MHV3-infected mice than in attenuated YAC-MHV3-infected mice. In vitro viral infections of interleukin (IL)-15-stimulated lymphoid cells from liver and bone marrow revealed that L2-MHV3 induced higher decreases in cell viability of NK1.1+ cells than the YAC-MHV3 variant. The NK cell decreases were due to the viral permissivity leading to cytopathic effects characterized by cell rounding, syncytia formation and apoptosis. Larger NK+ syncytia were observed in L2-MHV3-infected cells than in YAC-MHV3-infected cells. These results suggest that NK cell production is impaired by viral infection favouring fulminant hepatitis.

Animals↗
PubMed2001

Recovery from mouse hepatitis virus infection depends on recruitment of CD8(+) cells rather than activation of intrahepatic CD4(+)alphabeta(-)TCR(inter) or NK-T cells.

Mouse hepatitis virus (MHV) provides an excellent animal model for the study of the immunopathological mechanisms involved in hepatic viral diseases. We previously generated an attenuated viral variant, YAC-MHV3, which induces a subclinical disease and recovery within 15 days. In contrast, the L2-MHV3 strain induces the development of a fulminant hepatitis, leading to death within 3 days. In this paper, we document intrahepatic and splenic T cell subpopulations involved in the hepatitis process and viral elimination identified in attenuated or pathogenic MHV3-infected C57BL/6 mice. Percentages of intrahepatic CD4(+) cells decreased in attenuated YAC-MHV3-infected mice, while they increased in mice infected with pathogenic L2-MHV3, compared with uninfected animals. Moreover, in YAC-MHV3-infected mice, the percentages of intrahepatic CD8(+) cells slightly decreased at 24 h pi, then increased until 15 days pi. In contrast, the CD4/CD8 ratios of splenic lymphoid subpopulations increased in the first days of infection and returned to normal values at 15 days pi. Intrahepatic NK1.1(+)alphabeta - TCR(inter) cells decreased in both virally infected groups of mice, while CD4(+)alphabeta - TCR(inter) LFA-1(high) cells increased in L2-MHV3-infected mice, in contrast with what was seen in YAC-MHV3-infected mice. However, these cells became anergic following Con A or PHA stimulation. Ex vivo studies showed that only the intrahepatic CD8(+) cells that were increased in YAC-MHV3-infected mice could be stimulated by lectins. In addition, in vitro viral infections revealed that L2-MHV3 viral infection led to an increase of intrahepatic CD4(+)alphabeta - TCR(inter) cells in the absence of CD8(+) cells only. These results indicate that the attenuated phenotype of the YAC-MHV3 virus is related to two different mechanisms: the first involves no increase of intrahepatic CD4(+)alphabeta - TCR(inter) or NK-T cells, while the second favors the recruitment and activation of CD8(+) cells in liver. The results are discussed in relation to the integrity of intrahepatic immune tolerance mechanisms and immune-mediated viral elimination.

Animals↗
PubMed2001

Polyclonal activation of B cells occurs in lymphoid organs from porcine reproductive and respiratory syndrome virus (PRRSV)-infected pigs.

Porcine reproductive and respiratory syndrome virus (PRRSV) induces a persistent viral infection associated with an inefficient humoral immune response. A study of lymphoid B cells and specific humoral immune response was performed in blood and several lymphoid organs collected from PRRSV experimentally-infected pigs. Groups of specific pathogen-free (SPF) pigs were infected with the LHVA-93-3 isolate of PRRSV, and blood, tonsils, spleen and mediastinal lymph nodes (MLN) were collected at various times postinfection (p.i.) (3-60 days). Lymphoid cells were isolated, immunolabeled for cytofluorometric determination of B cell percentages, used for counting specific anti-PRRSV antibody secreting B cells by an ELISPOT assay, or cultured for metabolic activity. The presence of anti-PRRSV antibodies in the serum of infected pigs was determined using a commercial ELISA assay. Virus detection was performed in all tissues, including lungs, by virus isolation and RT-PCR. The results show that percentages of B cells increased in tonsils as soon as 3 days until 17 days p.i. in PRRSV-infected pigs while they increased in spleen at 3 days p.i. only, due to an increase of larger Ig(high)-producing B cells. Metabolic activity of lymphoid cells from blood and spleen increased at 3 days p.i. only while lymphoid cells from tonsils and MLN transiently decreased at that time and increased thereafter up to 60 days p.i. Anti-PRRSV antibody-secreting B cells occurred in tonsils after 10 days p.i. and strongly increased up to 60 days p.i. However, specific anti-PRRSV-secreting B cells were detected in blood and spleen after 17 days p.i and in MLN only after 45 days p.i. Specific antibodies were detectable in serum at 10 days p.i., reached the maximum level at 45 days and remained high up to 60 days p.i. Infectious virus was detected in lungs and MLN as soon as 3 days p.i., and remained detectable up to 45 days p.i. in tonsils of one pig while viral RNA was detected in most organs up to 60 days p.i. In vitro experiments revealed that inactivated virus induced a stimulation of lymphoid cells isolated from PRRSV-infected pigs while it was cytotoxic for lymphoid cells from control pigs. Taken together, these results indicate that viral infection induced simultaneously a polyclonal activation of B cells, mainly in tonsils, and an exaggerated and prolonged specific humoral immune response due to persistent viral infection in lymphoid organs.

Animals↗
PubMed2000

Dose-dependent apoptosis induced by low concentrations of methylmercury in murine splenic Fas+ T cell subsets.

Methylmercury chloride (MeHgCl) is known to induce cellular and humoral immunodeficiencies in mice. In this study, the involvement of lymphoid subset disorders due to low concentrations of methylmercury (0.001-1.0 microM) has been examined. Cytofluorometric analysis of splenic cells exposed in vitro to low concentrations of MeHgCl for 48 h revealed two distinct populations: the first expressed a typical lymphoid forward light scatter (FSC)/side light scatter (SSC) pattern (R1 region), and the second was characterized by a lower FSC and a higher SSC (R2 region). A dose-dependent shift of cells from R1 region toward R2 region was observed in splenic cells treated with MeHgCl. The apoptotic state of cells in the R2 region was confirmed by the TdT-mediated dUTP nick end labeling (TUNEL) assay. Analysis of DNA content in splenic lymphoid cells showed that low concentrations of MeHgCl increased both hypoploid cells and cells in G0-G1/S phase, both in the R1 and R2 regions. However, the numbers of cells in G0-G1/S and G2/M phases were decreased, but hypoploid cells increased in both regions due to exposure to 1 microM MeHgCl. MeHgCl-induced apoptosis disappeared when splenic cells were pretreated with anti-Fas antibodies, indicating that Fas expressing cells were the target cells for MeHgCl-mediated apoptosis. Furthermore, T cells from the V beta 8 family were found to be more sensitive to apoptosis induced by low concentrations of MeHgCl. Taken together, these results suggest that MeHgCl at low concentrations mediates the development of apoptosis in peripheral T cell via the Fas/FasL pathway.

Animals↗
PubMed2000

Experimental transmission of porcine circovirus type 2 (PCV2) in weaned pigs: a sequential study.

Weaned specific pathogen-free pigs were inoculated intranasally with porcine circovirus type 2 (PCV2) and killed in groups of two or three animals at 6, 13, 20, 27 and 34 days post-inoculation (dpi), together with appropriate uninfected controls, for examination by histopathological, immunohistochemical (immunogold silver staining; IGSS), polymerase chain reaction (PCR) and viral isolation techniques. Serum samples were also collected for detection of antibodies. No major clinical signs were observed in infected pigs, and gross lesions were essentially limited to the lungs and lymph nodes of some of the animals. Histologically, no lesions were seen at 6 dpi, but bronchointerstitial pneumonia was invariably noted from 13 dpi onwards. Granulomatous inflammation, with or without intracytoplasmic inclusions, was present in lymphoid tissues (e.g. lymph nodes, thymus, spleen and tonsil) from day 20 onwards, being most severe at days 20 and 27 dpi. Liver inflammation was present at days 13, 20 and 27 dpi. Virus was demonstrated in the tissues by isolation and PCR methods throughout the experiment. PCV2 antigens were detected by IGSS in bronchial and bronchiolar epithelial cells, in mononuclear cells and multinucleated giant cells within inflammatory lesions, and in mononuclear cells of apparently normal tissues (e.glamina propria of the small intestine and the bronchus-associated lymphoid tissue). The lesions were consistent with those of postweaning multisystemic wasting syndrome (PMWS), although not all previously reported PMWS lesions were seen. PCV2 antibodies were detected in infected pigs from day 13 onwards. The results demonstrated widespread distribution of PCV2 after infection and persistence of the virus in vivo for at least 34 days. It would appear that PCV2 can induce PMWS lesions in weaned pigs in the absence of porcine parvovirus and other common swine pathogens.

Animals↗
PubMed1999

Toxicity and bioaccumulation of nickel sulfate in Sprague-Dawley rats following 13 weeks of subchronic exposure.

Adult male Sprague-Dawley rats were given 0, 0.02, 0.05, and 0.1% nickel sulfate (NiSO4-6H2O) or 0, 44.7, 111.75, and 223.5 mg Ni/L, respectively, in their drinking water for 13 wk. Twenty-four hours following the end of such treatment, all animals survived and no apparent clinical signs of toxicity were noted. The final mean body weights of various nickel sulfate-treated rats were not significantly decreased except for the 0.1% nickel sulfate treated group when compared to those in the control. The absolute and relative organ weights were either increased or decreased or remained unchanged, depending on the organ and the dose of nickel sulfate. Total plasma proteins, plasma albumin and globulins, and plasma glutamic pyruvic transaminase activity were all significantly decreased in 0.1% nickel sulfate-treated rats. Lymphocyte subpopulations (T and B cells) were induced at lower dose levels, but suppressed at the highest (0.1%) dose group. A significant decrease in urine volume and an increase in BUN were observed at the highest dose group. Biochemical analysis of bronchoalveolar lavage fluid and lung tissue showed some lung damage, whereas no damage to the testis or DNA in liver and kidneys were found. No gross or microscopic changes were seen in any of the various tissues examined. The relative order of bioaccumulation of nickel in different organs of rats when treated at 0.1% nickel sulfate (223.5 mg Ni/L) was kidneys > testes > lung = brain > spleen > heart = liver. But with regard to order of toxicity, both immune and pulmonary systems were found to be very sensitive targets, followed by kidney.

Analysis of Variance↗
PubMed1998

Intrahepatic alpha beta-TcRintermediate LFA-1high T cells are stimulated during mouse hepatitis viral infection.

Mouse hepatitis virus type 3 (MHV3), a coronavirus, is an excellent animal model for the study of thymic and extrathymic T cell subpopulation disorders induced during the viral hepatitis. To understand local hepatic immune responses, the phenotypes of resident hepatic lymphocytes were determined and compared that of splenic and thymic T cell subpopulations during the acute viral hepatitis induced by MHV3 in susceptible C57BL/6 mice. Single positive (SP) CD4+ or CD8+ cells strongly increased in the liver. A specific cell population, the double positive (CD4+ C8+) cells, normally present in liver and thymic cell preparations, decreased in C57BL/6 mice following the viral infection. alpha beta-TcRintermediate T cells shifted toward alpha beta-TcRhigh T cells in the liver and thymus of infected mice, but not in their spleen. The specific alpha beta-TcRint or high lymphocytes occurring in the liver of MHV3-infected mice expressed higher levels of leukocyte function antigen-1 (LFA-1) and Pgp-1 (CD44) activation markers, suggesting that they were either activated or antigen-experienced during the viral infection. No significant changes in T cell subpopulations were detected in the spleen. These observations suggest that MHV3 infection could induce an early in situ stimulation of resident hepatic T cells, despite a peripheral immunodeficiency in the thymus and spleen.

Animals↗
PubMed1998

Clonal deletion of some V beta+ T cells in peripheral lymphocytes from C57BL/6 mice infected with MHV3.

Mouse hepatitis virus type 3 infection is generally accompanied by a severe immune dysfunction involving thymic or splenic T cell subpopulations. We postulate that the peripheral lymphoid cell depletions were caused by a selective deletion of some V beta subsets of mature T cells, as observed with superantigens. We have examined the expression of V beta 6, V beta 8 and V beta 14 in T cell subpopulations from the spleen and lymph nodes of pathogenic L2-MHV3-infected C57BL/6 mice. Cytofluorometric study showed decreases in splenic V beta 8+, V beta 6+, and V beta 14+ T cell subpopulations at 72 hrs post-infection. Single positive CD4+ T cells were diminushed but not the CD8+ cells. In contrast, the various V beta splenic cell populations were not modified in mice infected with a non- pathogenic YAC-MHV3 variant. However, the V beta 8/CD4 ratio increased in splenic cells but decreased in lymphocytes from lymph nodes. The V beta 14/CD4 ratio decreased only in splenic cells while V beta 6/CD4 ratios were not modified. These results suggest that alterations in V beta cell populations may play a role in the L2-MHV3-induced immunodeficiency.

Animals↗
PubMed1997

Mouse hepatitis viral infection induces an extrathymic differentiation of the specific intrahepatic alpha beta-TCRintermediate LFA-1high T-cell population.

Mouse hepatitis virus type 3 (MHV3), a coronavirus, is an excellent model for the study of thymic and extrathymic T-cell subpopulation disorders induced during viral hepatitis. It was recently reported that, in addition to the intrathymic T-cell differentiation pathway, an extrathymic differentiation pathway of alpha beta-T-cell receptor (TCR) T lymphocytes exists in the liver, and becomes important under pathological situations such as autoimmune diseases, malignancies or hepatic bacterial infections. In the present study, we compared the phenotypes of resident hepatic, splenic or thymic T-cell subpopulations during the acute viral hepatitis induced by HMV3 in susceptible C57BL/6 mice. The number of liver-resident mononuclear cells (MNC) increased during the viral infection, while cellularity decreased. Single positive (SP) CD4+ cells strongly increased in both the liver and thymus, while double positive (DP) (CD4+ CD8+) cells, present in the liver and thymus of mock-infected mice, decreased in C57BL/6 mice during the viral infection. A shift of alpha beta-TCRintermediate T cells toward alpha beta-TCRhigh was evidenced in the liver and thymus of infected mice, but not in the spleen. The few alpha beta-TCRint double negative (DN) (CD4-CD8-) cells also decreased following viral infection. alpha beta-TCRint or high lymphocytes expressing high levels of leucocyte function antigen-1 (LFA-1) increased in the liver of MHV3-infected mice. In addition, liver-resident T cells expressed strongly the CD44 (Pgp-1) activation marker, suggesting that they were either activated or antigen experienced during the viral infection. No significant change in T-cell subpopulations was detected in the spleen, suggesting that MHV3 infection could induce an early in situ differentiation of resident hepatic T cells rather than a recruitment of lymphocytes from peripheral lymphoid organs.

Animals↗
PubMed1996

Effect of adoptive transfer of CD4, CD8 and B cells on recovery from MHV3-induced immunodeficiencies.

A chronic viral infection can occur when the host fails to mount an effective immune response to clear the virus. Mouse hepatitis virus type 3 (MHV3) appears to be an excellent model for the study of the relationship between viral-induced immunodeficiency and chronic disease development. (C57BL/6 x A/J)F1 mice surviving acute hepatitis develop a chronic disease characterized by T- and B-cell immunodeficiencies, viral persistence in various organs including the brain, spleen and thymus, and death within 3 months postinfection (p.i.). We have reported that T- or B-cell deficiencies, observed in MHV3 chronically infected (C57BL/6 x A/J)F1 mice, can be partially or totally thwarted by adoptive transfer of CD4+, CD8+ and/or B cells, at 15 days p.i. in mice surviving the acute phase of the disease. Adoptive transfer of syngeneic CD4+ and/or CD8+ allowed a partial restoration of the T-cell deficiencies, as characterized by thymic atrophy, decrease in splenic T cells, and in all thymocyte subpopulations. B-cell immunodeficiency, as defined by a decrease in splenic B cells, as well as in the bone marrow pre-B- and B-cell compartments, and the occurrence of abnormally larger forms of bone marrow pre-B and B cells, were partially thwarted by B-cell treatment only. Splenic B cells and the bone marrow B-cell compartment, respectively, returned partially or totally to normal values, whereas the pre-B-cell compartment remained depleted in infected mice treated with B cells. Levels of all immunoglobulin classes returned to normal values in MHV3 chronically infected mice when treated with CD4+ in combination with CD8+ cells. All T- and/or B-cell treatments, however, were sufficient to thwart the process of the chronic disease, and favoured the survival of mice for up to 6 months p.i.

Animals↗
PubMed1995

T cell immunodeficiency involved in pathogenicity of attenuated MHV3 mutants.

Viral pathogenicity results when there is an imbalance between viral replication and the host's immune defenses. The immune system plays and important role in the outcome of an acute disease induced by the mouse hepatitis virus type 3 (MHV3). Of use in the study of the role of viral properties involved in its pathogenicity is the attenuated escape mutants. We reported that two MHV3 escape mutants were attenuated in their ability to deplete T cell subpopulations in the spleen in BALB/c mice according to inoculation route and time postinfection. The highly attenuated CL12 mutant cannot induce depletion in T cells following intraperitoneal (i.p.) or intranasal (i.n.) inoculations, at three days postinfection (p.i.). The less attenuated 51.6 mutant, however, maintained the ability to deplete T cells following i.p. inoculation, as described for the pathogenic MHV3. In contrast, no depletion of T cells following i.n. inoculation was induced with this mutant. The use of such mutants enables us to dissect the role of each compartment of the immune system.

Animals↗
PubMed1995

Impairment of bone marrow pre-B and B cells in MHV3 chronically-infected mice.

Mouse hepatitis virus type 3 (MHV3) appears to be an excellent model for the study of the relationship between viral-induced immunodeficiency and the development of chronic disease. Animal surviving acute hepatitis develop a chronic disease characterized by viral persistency in various organs, by a humoral immunodeficiency, and eventually die within the next three months postinfection. To verify if B cell immunodeficiency occurs during the chronic disease, percentage and absolute number of bone marrow B lineage cell subpopulations were recorded at various times postinfection (p.i.) in pathogenic L2-MHV3-infected (C57BL/6 x A/J) F1 mice. Absolute numbers of B (cmu+smu+) cells decreased as early as three days p.i. up to 15 days p.i., and then gradually returned toward normal values in L2-MHV3-infected mice during the chronic disease. In contrast, pre-B (cmu+smu-) cells were less significantly decrease during the chronic disease. In addition, abnormally enlarged cells (> 13 microns) were detected either in bone marrow pre-B or B cells from L2-MHV3-infected mice.

Animals↗
PubMed1994

Impaired T and B cell subpopulations involved in a chronic disease induced by mouse hepatitis virus type 3.

A chronic viral infection can occur when the host immune system fails to detect the viruses. Mouse hepatitis virus type 3 (MHV3) seems to be an excellent model for the study of the relationship between viral-induced immunodeficiency and the development of chronic disease. Animals that survive acute hepatitis develop a chronic disease characterized by viral persistency in various organs, including the brain, spleen, and thymus, and they eventually die within the next 3 mo postinfection (p.i.). To verify whether T and B cell immunodeficiency occurs either in the acute or chronic phase of the disease, the percentage and absolute number of splenic T and B lymphocytes, thymic T, or bone marrow B-lineage cell subpopulations were recorded at various times p.i. in pathogenic L2-MHV3-infected and nonpathogenic YAC-MHV3-infected (C57BL/6 x A/J) F1 mice. Splenic T and B cells were depleted as early as 48 h p.i., and maintained at low levels for up to 3 mo until death of mice. Such depletions resulted from thymic depletion in all T cell subpopulations, and in B (cytoplasmic micro-chain+ and surface micro-chain+) lymphocytes only in the bone marrow of pathogenic L2-MHV3-infected mice. In vitro studies of purified thymic stromal cells have produced a nonproductive L2-MHV3 replication with a low viral transmission to complexed thymocytes. However, pre-B and B cells have supported a productive viral replication, generating abnormal forms, which leads to cell lysis. These results are discussed in relation to viral persistency in the brain and lymphoid cells, which results from a chronic impairment of cellular and humoral immune mechanisms that are involved in the viral elimination process.

Animals↗
PubMed1994

Herpes simplex virus type 1 pathogenicity in mice expressed by lytic infection in pre-B and B cells.

The outcome of herpes simplex virus type 1 (HSV-1) infection in human or in the murine model can be influenced by host immunocompetency. We postulate in this work that HSV-1 infection alters bone marrow B lymphopoiesis in genetically determined susceptible mice. To verify this hypothesis, resistant C57BL/6 or susceptible A/J adult mice were intraperitoneally infected with HSV-1 (McIntyre strain). At various postinfection times, spleen and bone marrow were collected from both infected mouse strains. B lineage cell subpopulations were identified by double immunofluorescence assays using mAbs to terminal deoxynucleotidyl transferase (TdT), 220-kDa surface membrane glycoprotein (detected by mAb 14.8), and cytoplasmic (c mu) or surface (s mu) IgM chains. Results revealed a decrease in both percentage and absolute number of splenic B (c mu+, s mu+) cells and bone marrow pre-B (c mu+, s mu-) and B cells isolated only from susceptible A/J mice. No effect was observed on pro-B (14.8+, c mu-) or TdT+ precursor cells from both mouse strains. Intracellular viral proteins were detected in pre-B and B cells in in vivo-infected susceptible A/J mice. In vitro studies also revealed that virus-induced cell lysis occurred in purified splenic and bone marrow pre-B or B cells derived only from susceptible A/J mice. Viral tropism for pre-B and B cells represents another immunodeficiency mechanism involved in the genetic sensitivity to HSV-1.

Animals↗
PubMed1994

Pathogenicity of neutralization escape mutants of mouse hepatitis virus: correlation with T- and B-cell depletions.

Viral pathogenicity is a result of an imbalance between viral replication and the host's immune defences. When the virus is lymphotropic, understanding the pathogenic process of the viral disease becomes complicated because virus/lymphocyte interactions can alter the cell's integrity and subsequently induce immunodeficiency. The immune system plays an important role in the outcome of acute disease induced by the mouse hepatitis virus type 3 (MHV3). The use of attenuated escape mutants provides a tool to study the role of viral properties involved in its pathogenicity. We selected MHV3 mutants by virtue of their resistance to neutralization by monoclonal antibodies (mAb), in order to study their pathogenic properties. We reported that two MHV3 escape mutants were attenuated in their pathogenic properties according to inoculation site and with regard to survival time and ability to deplete T- and B-cell subpopulations in the spleen, thymus and bone marrow of susceptible Balb/c mice. The highly attenuated CL12 mutant could not induce depletion in T or B cells following intraperitoneal (i.p.) or intranasal (i.n.) inoculations, at three days postinfection. The less attenuated 51.6 mutant, however, maintained the ability to deplete T and B cells following i.p. inoculation, as described with the pathogenic MHV3. In contrast, no depletion of T cells following i.n. inoculation was induced with this mutant, although B lineage cells decreased. The use of such mutants enabled us to examine the role of each compartment of the immune system, since the highly attenuated CL12 mutant induced no immunodeficiency, as defined by immune cell depletion, whereas the less attenuated 51.6 mutant maintained its ability to decrease only the B-cell compartment after i.n. inoculation. Results are discussed with regard to the virus/lymphocyte interactions during the pathogenic process.

Administration, Intranasal↗
PubMed1994

Low-virulent mouse hepatitis viruses exhibiting various tropisms in macrophages, T and B cell subpopulations, and thymic stromal cells.

Functional or cellular immunodeficiencies have been reported to result from various pathogenic mouse hepatitis virus (MHV) strains. Moreover, low-virulent MHV strains can reduce the ability of mice to seroconvert to other antigens or viruses. To determine the importance of low-virulent MHV strain tropism in immune cells, as a mechanism involved in the induction of immunodeficiencies, peritoneal exudate cells, T and B cell subpopulations, and thymic stromal cells were infected with low-virulent MHV-D, MHV-K, and MHV-N and pathogenic MHV-3 viral strains. Cell viability, percentages of viral protein-expressing cells, and virus titers have been analyzed. On the basis of our findings, low-virulent MHV viral strains exhibit various tropisms in macrophages, B lymphocyte subpopulations, or thymic stromal cells when compared with the more virulent MHV-3 serotype. All MHV strains tested have replicated in peritoneal exudate cells of C57BL/6 or A/J mice. Low-virulent MHV-N and pathogenic MHV-3 strains showed higher tropism for peritoneal exudate cells than low-virulent MHV-K and MHV-D strains. Likewise, MHV-N and -3 serotypes expressed higher tropism than MHV-D or -K serotypes for thymic stromal cells and B lymphoid cells. No tropism for T lymphocytes, however, was detected with MHV except when in contact with previously infected thymic stromal cells. These results raise the problem of immunologic disorders resulting from viral replication in immune cells in mouse colonies subclinically infected with low-virulent MHV strains.

Animals↗
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↗