Résumé Le chitosane est une molécule retrouvée naturellement dans les carapaces de crustacés mar... more Résumé Le chitosane est une molécule retrouvée naturellement dans les carapaces de crustacés marins. Les dérivés obtenus par hydrolyse de cette molécule possèdent plusieurs propriétés biologiques intéressantes au niveau nutraceutique. Des expériences dans un modèle murin ont permis de déterminer les effets de l’utilisation journalière par voie orale de la poly-glucosamine (Oligo-Flex MD) pour la prévention de l’ostéoarthrite inflammatoire expérimentale. Les
The outcome of herpes simplex virus type 1 (HSV-1) infection in human or in the murine model can ... more 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.
A chronic viral infection can occur when the host immune system fails to detect the viruses. Mous... more 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.
Functional or cellular immunodeficiencies have been reported to result from various pathogenic mo... more 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.
A chronic viral infection can occur when the host immune system fails to detect the viruses. Mous... more 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.
Functional interaction between lymphoid cells and lymphotropic viruses is particularly evident fo... more 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)
Mouse hepatitis virus type 3 (MHV3) provides an excellent model for studying viral-B lymphocyte i... more 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.
Functional or cellular immunodeficiencies have been reported to result from various pathogenic mo... more 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.
Mouse hepatitis virus type 3 (MHV3) appears to be an excellent model for the study of the relatio... more 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.
Résumé Le chitosane est une molécule retrouvée naturellement dans les carapaces de crustacés mar... more Résumé Le chitosane est une molécule retrouvée naturellement dans les carapaces de crustacés marins. Les dérivés obtenus par hydrolyse de cette molécule possèdent plusieurs propriétés biologiques intéressantes au niveau nutraceutique. Des expériences dans un modèle murin ont permis de déterminer les effets de l’utilisation journalière par voie orale de la poly-glucosamine (Oligo-Flex MD) pour la prévention de l’ostéoarthrite inflammatoire expérimentale. Les
The outcome of herpes simplex virus type 1 (HSV-1) infection in human or in the murine model can ... more 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.
A chronic viral infection can occur when the host immune system fails to detect the viruses. Mous... more 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.
Functional or cellular immunodeficiencies have been reported to result from various pathogenic mo... more 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.
A chronic viral infection can occur when the host immune system fails to detect the viruses. Mous... more 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.
Functional interaction between lymphoid cells and lymphotropic viruses is particularly evident fo... more 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)
Mouse hepatitis virus type 3 (MHV3) provides an excellent model for studying viral-B lymphocyte i... more 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.
Functional or cellular immunodeficiencies have been reported to result from various pathogenic mo... more 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.
Mouse hepatitis virus type 3 (MHV3) appears to be an excellent model for the study of the relatio... more 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.
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