concanavalin-a and Cytomegalovirus-Infections

Topics: Cells, Cultured; Concanavalin A; Creatinine; Cytomegalovirus; Cytomegalovirus Infections; Ganciclovir; Humans; Immunosuppressive Agents; Kidney Transplantation; Leukocytes; Polymerase Chain Reaction; Postoperative Complications; T-Lymphocytes

Virus-monocyte interactions were evaluated in patients with mononucleosis due to cytomegalovirus (CMV). Group 1 patients studied about two weeks after the onset of symptoms had lymphocyte responses to concanavalin A (con A) that were maximally suppressed and unaffected by in vitro culture or reconstitution with monocytes. Lymphocytes from group 2 patients studied about three weeks after the onset of symptoms had less markedly suppressed responses, which were reversed by in vitro culture or by reconstitution with monocytes. Monocyte depletion resulted in a marked diminution of fresh lymphocyte responses of group 2 patients but not of group 1 patients. CMV was isolated from blood monocytes of four patients with mononucleosis; intact, infected monocytes were capable of suppressing responses of cultured autologous lymphocytes to con A. Monocytes from uninfected control donors were infected in vitro with CMV and evaluated for the induction of suppressor activity. CMV-infected monocytes were significantly more suppressive for autologous lymphocyte responses to con A than were uninfected monocytes.

Topics: Adult; Aged; Concanavalin A; Cytomegalovirus; Cytomegalovirus Infections; Humans; Immune Tolerance; Infectious Mononucleosis; Lymphocyte Activation; Middle Aged; Monocytes; Virus Replication

CD4 T cells are important regulators of the immune system and are vital for mounting a strong immune response against viral infections. Human cytomegalovirus (HCMV) is known to be a strong modulator of the innate as well as adaptive immune responses. In this study, we found that HCMV directly inhibited proliferation of CD4 T cells and rendered them unresponsive to immunological stimuli. This effect was not observed when CD4 T cells were treated with herpes simplex virus-1/2 or measles virus. When stimulated with phytohemagglutinin, concanavalin A, or phorbol myristate acetate, HCMV-treated T cells were unable to proliferate, revealing an ability of HCMV to inhibit CD4 T cell response. Furthermore, HCMV also prevented proliferation of leukemic T-cell lines. HCMV-treated CD4 T cells expressed the activation markers CD45RO and CD69, were not apoptotic and produced decreased levels of the cytokines IL-4, IFN-γ and TNF-α, compared to untreated controls. The inhibitory effect of HCMV on CD4 T cell proliferation was not mediated by HCMV gH, gB or other immunogenic glycoproteins, since intravenous immunoglobulins or gB- or gH-specific neutralizing antibodies did not prevent the suppression of T-cell proliferation. Our observations show that HCMV inhibits CD4 T cell function with potential clinical consequences for both humoral and cell-mediated immune responses.

Topics: Antibodies, Viral; Antigens, CD; Antigens, Differentiation, T-Lymphocyte; CD4-Positive T-Lymphocytes; Cell Line, Tumor; Cell Proliferation; Concanavalin A; Cytomegalovirus; Cytomegalovirus Infections; Herpesvirus 1, Human; Herpesvirus 2, Human; Humans; Interferon-gamma; Interleukin-4; K562 Cells; Lectins, C-Type; Leukocyte Common Antigens; Leukocytes, Mononuclear; Lymphocyte Activation; Macrophages; Measles virus; Phytohemagglutinins; Tetradecanoylphorbol Acetate; Tumor Necrosis Factor-alpha

Antiviral prophylaxis against cytomegalovirus has been associated with reduced risk of allograft rejection and improved allograft survival after renal transplantation. This phenomenon might not be fully explained by preventing the indirect effects of cytomegalovirus. The effect of antiviral agents on lymphocyte function in patients treated with modern immunosuppression has not been studied to date.. Adult renal transplant recipients were assigned to 3-month prophylaxis with either valganciclovir (900 mg once daily; n=19) or valacyclovir (2 g four times daily; n=17) as part of an ongoing randomized trial. Subsets of lymphocytes, lymphocyte proliferation and/or cytokine production after in vitro mitogen stimulation were evaluated at the end of prophylaxis and 1 month after withdrawal of antiviral drugs.. Lymphocyte proliferation was significantly decreased both after phytohemagglutinine (25% ±15% versus 32% ±18%; P=0.025) and concanavalin A stimulation (17% ±9% versus 25% ±16%; P=0.011) during valganciclovir, but not valacyclovir therapy. Moreover, a lower activated T-cell count (CD3(+)HLA-DR(+) cells) was noted in valganciclovir-treated patients (13% ±10% versus 17% ±12% of total CD3(+) T-cells; P=0.005).. Valganciclovir suppresses lymphocyte proliferation and activation in patients after renal transplantation.

Topics: Acyclovir; Adult; Antiviral Agents; Cell Proliferation; Cells, Cultured; Concanavalin A; Cytomegalovirus; Cytomegalovirus Infections; Female; Ganciclovir; Graft Rejection; Graft Survival; Humans; Immunosuppression Therapy; Immunosuppressive Agents; Kidney Transplantation; Lymphocyte Activation; Lymphocyte Count; Male; Middle Aged; Phytohemagglutinins; T-Lymphocyte Subsets; Valacyclovir; Valganciclovir; Valine

Profound T-cell depletion with the monoclonal antibody alemtuzumab facilitates reduced maintenance immunosuppression in abdominal and lung transplantation. While the phenotype of the post-depletional T cells has been characterized, little is known about their function. In the present study, global and CMV-specific T-cell function was assessed longitudinally in 23 lung transplant (LTx) recipients using T-cell assays (ImmuKnow and T Cell Memory, Cylex, Columbia, MD) during the first year posttransplant after induction therapy. Recovery of mitogen responses were seen at 2 weeks posttransplantation (65%PHA; 58% Con A), despite the low number of circulating T cells (<2%). These responses declined at 4-5 months (24%PHA; 54% Con A) and were partially reconstituted by 9 months (46% PHA; 73% Con A). CMV-specific responses recovered in 80% of R+ patients as early as 2 weeks posttransplant (n = 5) and 72% of patients had a memory response by 3 months (n = 11). In contrast, only 2 of 5 patients who did not exhibit memory responses pre-transplant (R-) developed transient CMV-specific T-cell responses. Our results show that profound depletion of T cells induced by alemtuzumab spares the functional subset of CMV-specific memory T cells. Conversely, CMV R- patients predepletion may require a prolonged period of prophylaxis.

Topics: Alemtuzumab; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antibodies, Neoplasm; Concanavalin A; Cytomegalovirus; Cytomegalovirus Infections; Humans; Immunologic Memory; Immunosuppression Therapy; Longitudinal Studies; Lung Transplantation; Lymphocyte Depletion; Mitogens; Phytohemagglutinins; Risk Factors; T-Lymphocyte Subsets

Mitogen concanavalin A (ConA) response and cytomegalovirus (CMV)-specific memory response were assessed in 24 liver transplant recipients and compared with healthy subjects. Transplant recipients as compared to healthy subjects had a lower CMV memory response at 2 weeks (P=0.023), and at 1 month (P=0.06), but a comparable response at 3 months. CMV recipient+/donor+(R+/D+) patients had the greatest increase in CMV-specific memory response at 2-3 months as compared to all other groups. Within this R+/D+ group, CMV-specific memory response was significantly more robust in patients who never had CMV infection as compared to those who developed CMV infection (P=0.035). ConA response at 2 weeks was significantly lower in patients with major infections as compared to those without them (SI 5.4 vs. 38.1, P=0.039). Thus, reconstitution of CMV-specific T-helper cell response was distinct for subsets of liver transplant recipients based on the recipient and donor CMV serostatus. Impairment in proliferative response to ConA identified a subgroup of patients with major infections after liver transplantation.

Topics: Antibodies, Viral; Concanavalin A; Cytomegalovirus; Cytomegalovirus Infections; Humans; Immunologic Memory; Liver Transplantation; Lymphocyte Activation; T-Lymphocytes, Helper-Inducer; Tissue Donors

Murine cytomegalovirus infection of spleen cultures induced the production of a small (less than 10,000 molecular weight) immunosuppressive factor (VISF), which suppressed concanavalin-A mitogenesis in fresh mouse spleen cells, and in fresh human peripheral blood leukocytes. The factor did not affect the growth of two murine T-cell lines or of mouse fibroblasts. A similar factor was also found in the serum of infected mice, at the time of maximum immune suppression. The properties of VISF indicate that the mechanism of MCMV immune suppression is different from that caused by several other viruses which are important in human and veterinary medicine.

Topics: Animals; Cell Division; Cell Line; Cells, Cultured; Chromatography; Concanavalin A; Cytomegalovirus; Cytomegalovirus Infections; DNA; Humans; Immunosuppressive Agents; Lymphocyte Activation; Lymphocytes; Mice; Spleen; Thymidine; Viral Proteins

An experimental model for testing antiviral agents against severe cytomegalovirus (CMV) infection in immunocompromised hosts was developed. The model consisted of cyclophosphamide (Cy) treatment of CMV-infected guinea pigs to simulate CMV infection in immunodeficient individuals. Of the 3 Cy regimens tested, a single 300 mg/kg dose administered one day after virus inoculation resulted in the most severe CMV infection considering mortality rates, mean day of death and loss of body weight. Evaluation of responses to both T and B cell mitogens suggested that the severe and lethal CMV infection resulted from the combined immunosuppressive effect of Cy and CMV. The nucleoside analog [9-(1-3-dihydroxy-2-propoxymethyl)guanine (DHPG) was used to assess the usefulness of the CMV-infected immunocompromised host model. DHPG (100 mg/kg/day for 8 days) prevented death but did not reduce virus infectivity titers in blood of Cy-treated, CMV-infected guinea pigs. This model of CMV infection in immunocompromised guinea pig is a relevant and convenient experimental tool for the assessment of candidate anti-CMV agents under well-defined experimental conditions, such as appropriate CMV inoculum and Cy regimen.

Topics: Acute Disease; Animals; Antiviral Agents; Cells, Cultured; Concanavalin A; Cyclophosphamide; Cytomegalovirus Infections; Disease Models, Animal; Dose-Response Relationship, Drug; Female; Ganciclovir; Guinea Pigs; Immunologic Deficiency Syndromes; Lymphocyte Activation

Spleen cells from mice infected with virulent and avirulent strains of murine cytomegalovirus showed depressed interleukin-2 production after ConA stimulation. Cell-mixing experiments indicated that this was due to a primary defect in non adherent cells. Spleen cells infected in vitro were also studied.

Topics: Animals; Concanavalin A; Cytomegalovirus Infections; Immune Tolerance; Interleukin-2; Lymphocyte Activation; Mice; Spleen; T-Lymphocytes; Time Factors

Cytomegalovirus causes T cell immune impairment in infected mice, reflected by a decreased response to the T cell mitogens PHA and Con A, and reduction of Con A-induced IL-2 secretion. Concomitantly, a marked increase in the spleen weight of infected mice was found. Histological examination of the liver revealed focal hepatitis. These signs of infection lasted from day 5 to day 14 after infection when mice slowly started to recover. Systemic treatment of MCMV-infected mice with thymic humoral factor (THF) resulted in a reconstitution of the mitogenic responses, IL-2 secretion, normalization of spleen weight and recovery of liver inflammation. Unlike other thymic hormones, THF did not affect interferon synthesis and NK cytotoxicity in infected mice. It is concluded that THF restores immune competence of mice immunosuppressed as a result of MCMV infection, through modulation of the T cell compartment.

Topics: Animals; Concanavalin A; Cytomegalovirus Infections; Cytotoxicity, Immunologic; Female; Immune Tolerance; Interferons; Interleukin-2; Killer Cells, Natural; Lymphocyte Activation; Mice; Mice, Inbred BALB C; Phytohemagglutinins; Spleen; Thymus Hormones

Murine cytomegalovirus (MCMV) infection of mice resulted in suppression of mitogen induced proliferation and interleukin 2 (IL-2) responses of splenic cells. This suppression was also evident as a reduction in the number of cells expressing Thy-1 or L3T4 and a reduction in the ratio of T helper/T suppressor cells. The pyrimidinone compound, bropirimine, when administered to MCMV infected mice was able to restore mitogen-induced proliferative and IL-2 responses of splenic cells, to increase the number of cells expressing Thy-1 or L3T4, to restore the ratio of T helper/T suppressor cells and to increase the number of cells inducible for expression of IL-2 receptors.

Topics: Animals; Cell Division; Concanavalin A; Cytomegalovirus Infections; Cytosine; Female; Immune Tolerance; Interleukin-2; Lymphocyte Activation; Mice; Mice, Inbred BALB C; T-Lymphocytes

Murine cytomegalovirus infection in spleen cultures resulted in the production of a soluble factor, VISF (virus-induced suppressive factor), which inhibited concanavalin A mitogenesis in fresh spleen cells. Its production was specific for MCMV, since infection of spleen cultures by Sindbis virus, or bacteriophages PM 2 and T 4, and the phagocytosis of latex beads, all failed to elicit VISF. Maximum appearance of the factor occurred within 24 hours p.i. in spleen cultures, and its source was identified as the population of spleen cells which adhered to a plastic culture dish within two hours at 37 degrees C. Non-adherent cells did not produce the factor. Its production was not inhibited by indomethacin. VISF could be concentrated by ultrafiltration on a YM 2 membrane filter, and it was readily fractionated by chromatography on sephadex G-25. In relation to peptides of known molecular weight it appeared to be smaller than 1,400 daltons. Its ability to suppress concanavalin A mitogenesis was largely removed by digestion with proteinase K. Thus VISF appears to be a relatively small peptide or peptide-containing substance. It was purified further by HPLC.

Topics: Animals; Cells, Cultured; Chromatography, Gel; Chromatography, High Pressure Liquid; Concanavalin A; Cytomegalovirus; Cytomegalovirus Infections; Immune Tolerance; Indomethacin; Lymphocyte Activation; Mice; Peptides; Spleen; Ultrafiltration

A cytotoxic response to murine cytomegalovirus (MCMV) was obtained by the culture of lymph node cells from mice inoculated with MCMV into both hind footpads 7 days previously. The cytotoxicity was mediated by Thy1.2+, Lyt2+, H-2-restricted effector cells and was virus-specific. Investigation of the in vitro conditions established that T cell proliferation was necessary for optimal generation of cytotoxicity, that proliferation was dependent upon Thy1.2+, Lyt2+ cell populations and that supernatants from concanavalin A-activated spleen cells enhanced the levels of cytotoxicity obtained.

Topics: Animals; Antilymphocyte Serum; Complement System Proteins; Concanavalin A; Cytomegalovirus Infections; Cytotoxicity, Immunologic; Female; In Vitro Techniques; Lymph Nodes; Mice; Mice, Inbred BALB C; Mice, Inbred CBA; Spleen; T-Lymphocytes, Cytotoxic; Temperature

The following findings were noted among 45 bone marrow transplant recipients. The patients without cytomegalovirus (CMV) infection or chronic graft-versus-host disease (GVHD) showed normal lymphocyte stimulation in vitro by concanavalin A (Con A) more than 3 months after transplantation, and normal stimulation by phytohemagglutinin (PHA), anti-beta 2-microglobulin (A-beta 2m) and protein A (SpA) after 6 months. In contrast, the patients who had CMV infection without chronic GVHD had Con A and SpA responses within the normal range after 12 months and reduced lymphocyte responses to PHA and A-beta 2m more than 12 months after transplantation. The patients with chronic GVHD had reduced responses to all of these four mitogens after more than 12 months. In comparison with other patients those who later developed chronic GVHD showed an increased mixed lymphocyte culture stimulation during the first 3 months that decreased between 6-12 months. Patients with chronic GVHD still had reduced IgA levels at 12 months after transplantation. Patients with CMV infection, but without chronic GVHD, had higher percentages of lymphocytes with surface membrane Ig than healthy controls during the first 3 months after transplantation. The data suggest that CMV infection, regardless of chronic GVHD, delays immunologic recovery after marrow transplantation.

Topics: Antigens, Surface; beta 2-Microglobulin; Bone Marrow Transplantation; Concanavalin A; Cytomegalovirus Infections; Graft vs Host Disease; Humans; Immunoglobulins; Lymphocyte Activation; Lymphocyte Culture Test, Mixed; Phytohemagglutinins; Staphylococcal Protein A

Herpesviral infections and cellular immunity were studied in 19 patients with acquired immunodeficiency syndrome who were treated with human lymphoblastoid interferon for Kaposi's sarcoma. Before treatment, cytomegalovirus (CMV) and Epstein-Barr virus were isolated from 18 of 19 patients and 13 of 14 patients, respectively. Serum levels of interferon were measurable in all cases. Concanavalin A induced lymphocyte proliferation normally in 16 of 18 patients, but CMV induced proliferation in only nine of 18 patients. Natural killer cell activity was normal in 12 of 19 patients and was augmented in vitro by interferon in six of 19 subjects. CMV-specific HLA-restricted cytotoxic T cell activity was found in only two of 15 cases. With therapy, serum levels of interferon increased in 15 of 18 patients. There were two partial tumor remissions but no improvements in viral infections. Natural killer cell activity was decreased in 11 of 14 cases, and in vitro augmentation by interferon was absent in all five previous responders. CMV-specific T cell activity did not improve, but HLA-unrestricted cytotoxicity was increased in four of eight cases.

Topics: Acquired Immunodeficiency Syndrome; Adult; Antibodies, Viral; Antigens, Viral; Capsid Proteins; Concanavalin A; Cytomegalovirus; Cytomegalovirus Infections; Cytotoxicity, Immunologic; Herpesviridae Infections; Herpesvirus 4, Human; Homosexuality; Humans; Interferon Type I; Killer Cells, Natural; Lymphocyte Activation; Male; Middle Aged; Sarcoma, Kaposi

To study the effects of cytomegalovirus infection on T-lymphocyte subpopulations, we determined helper (Lyt 1.2) and suppressor (Lyt 2.2) T-lymphocyte subset numbers using monoclonal antibodies and measured lymphocyte responsiveness to mitogen during sublethal murine cytomegalovirus (MCMV) infection of 3-wk-old Balb/c mice. MCMV-infected mice had reduced Lyt 1.2 to Lyt 2.2 T-lymphocyte ratios on days 1, 3, 5, and 9 of infection. Alterations in T-lymphocyte subsets were accompanied by diminished lymphocyte response to concanavalin A. Lymphocyte responsiveness and Lyt 1.2 to Lyt 2.2 ratios were maximally reduced on day 5 of MCMV infection and correlated strongly with peak virus recovery from spleen, bone marrow, and peripheral blood leukocytes. These results indicate that acute MCMV infection of mice causes abnormalities in T-lymphocyte subset ratios and responsiveness to mitogen similar to the abnormalities observed in human cytomegalovirus infections. MCMV infection of mice is a useful model to study the mechanism by which cytomegalovirus infections induce altered T-lymphocyte subpopulations.

Topics: Animals; Antibodies, Monoclonal; Concanavalin A; Cytomegalovirus Infections; Female; Leukocyte Count; Mice; Mice, Inbred BALB C; T-Lymphocytes; T-Lymphocytes, Helper-Inducer; T-Lymphocytes, Regulatory

The nonspecific functional capacity of spleen cells, taken from female guinea pigs with primary acute cytomegalovirus (CMV) infection, was assessed using lipopolysaccharide (LPS), a B-cell mitogen, and concanavalin A (Con A), a T-cell mitogen. Proliferative responses to the two mitogens were found to be significantly depressed in animals inoculated with CMV as compared to control animals. The defect in Con A responsiveness occurred earlier during the course of the infection than the defect in LPS responses. Although responses to the mitogens were depressed at the time of peak virus activity in the spleen, the possibility of lytic destruction of the spleen cells by the virus during in vitro culture was excluded. In addition, the depression in Con A responsiveness was noted with a wide range of Con A concentrations, and preculture studies failed to result in enhanced reactivity of the cells from infected animals. We conclude that reductions of both B- and T-cell functions, which differ in their timing during the course of acute CMV infection, occur concurrently with an enhanced viral specific immune response in guinea pigs acutely infected with CMV.

Topics: Animals; B-Lymphocytes; Concanavalin A; Cytomegalovirus Infections; Guinea Pigs; Immune Tolerance; Lymphocyte Activation; Mitogens; Spleen; T-Lymphocytes

Immunoregulation of lymphocyte blastogenesis was studied in 13 patients with acute-phase cytomegalovirus (CMV) mononucleosis and 9 of these patients during the convalescent phase of the illness. Peripheral blood mononuclear leukocytes from acute-phase patients displayed depressed uptake of [3H-]thymidine in response to the lectin-mitogen concanavalin A (Con A) and immune-specific viral antigens (CMV, herpes simplex virus (HSV), mumps virus) compared with convalescent patients or normal donors. Removal of plastic-adherent cells from the patients' samples resulted in further depression of lymphocyte blastogenesis to Con A and CMV and HSV antigens, suggesting a helper function for the predominantly monocytic, adherent cell population in this response. Preliminary culture of mononuclear leukocytes from acute-phase patients for 18 hr at 37 degrees C resulted in significantly enhanced blastogenesis to Con A. In sharp contrast, lymphocyte blastogenesis to viral antigens was not significantly enhanced after preculture. These results suggest that different mechanisms are operative in immunoregulation of lymphocyte recognition responses to the polyclonal activator Con A and immune-specific viral antigens during human CMV infection.

Topics: Acute Disease; Adult; Antigens, Viral; Cells, Cultured; Concanavalin A; Cytomegalovirus; Cytomegalovirus Infections; Female; Humans; Immune Tolerance; Infectious Mononucleosis; Lymphocyte Activation; Male; Middle Aged; Monocytes

The mechanism of murine cytomegalovirus-induced immunosuppression was investigated by examining the roles played by lymphocytes and adherent cells derived from spleens of infected SWR/J mice. As few as 100 infected cells per spleen were correlated with complete abrogation of mitogen responses at 4 and 5 days after infection. In a series of cell mixing experiments it was shown that the deficiency in infected spleens was due partly to the adherent cells, which apparently secreted an immunosuppressive factor, and partly to the infected lymphocytes, which upon exposure to this factor could no longer respond to concanavalin A presented to them by normal adherent cells.

Topics: Animals; Concanavalin A; Cytomegalovirus; Cytomegalovirus Infections; Female; Immune Tolerance; Lipopolysaccharides; Lymphocyte Activation; Lymphocytes; Macrophages; Mice

Groups of mice that received a predominantly lethal or a nonlethal dose of murine cytomegalovirus (CMV) were studied prospectively to correlate clinical observations with detection of virus in spleen cells and with the response of spleen cells to the thymus-derived (T-) cell mitogen concanavalin A (con A). In both groups of mice, virus was virtually cleared from spleen cells by day 8 after infection. Depression of the spleen cell response to con A preceded clinical signs of infection, was more severe in the lethally infected group, and improved as clinical signs cleared in the few surviving mice. Serum from infected mice depressed the response of uninfected spleen cells to con A. These findings support the hypothesis that clinical illness and death from CMV infection of mice are a consequence of events that follow the depression of T-cell function by CMV. This depression is at least partially mediated by a humoral mechanism.

Topics: Animals; Concanavalin A; Cytomegalovirus; Cytomegalovirus Infections; Female; Immune Sera; Mice; Mice, Inbred DBA; Spleen; T-Lymphocytes

The suppression of T-cell deoxyribonucleic acid (DNA) synthesis by serum from mice acutely with murine cytomegalovirus (MCMV) was investigated. Spleen cells from uninfected mice were exposed to concanavalin A in the presence of serum taken from mice at various times after infection with MCMV. The capacity of the serum to suppress DNA synthesis first appeared at day 3 postinfection and was associated with free infectious virus. Addition of MCMV to serum from uninfected mice also suppressed DNA synthesis. Ultracentrifugation of serum from mice acutely infected with MCMV removed most of the virus and aborgated the inhibition of DNA synthesis. However, in two of four experiments, serum from mice in weeks 4 and 5 postinfection did not contain infectious MCMB but did suppress. Therefore, it appears that MCMV itself can suppress DNA synthesis of T cells; however, this may not be the exclusive mechanism of suppression exerted by serum from MCMB-infected mice.

Topics: Animals; Blood; Concanavalin A; Cytomegalovirus; Cytomegalovirus Infections; DNA; Female; Immune Sera; In Vitro Techniques; Mice; Spleen; T-Lymphocytes

Both in vitro and in vivo murine cytomegalovirus (MCMV) infection depressed the responses of lymphocytes to both B and T cell mitogens. The possibilities that macrophages or nonspecific T cell inhibition of B cells might account for the depressed responses were eliminated. In vitro data suggested that B cell responses are more susceptible to this depression than T cell responses. The possibility that the depression of T cell responses is not a direct effect of viral infection of lymphocytes is discussed. To investigate further the interaction between B and T lymphocytes and MCMV, mice with B and T cell deficiences were studied. A comparison of the susceptibility of athymic Nu/Nu mice and T cell competent Nu/+ littermates to MCMV showed that the LD50 for Nu/Nu mice is 10-fold lower than that for Nu/+ mice, but Nu/+ mice given an LD50 of virus died much sooner after infection than Nu/Nu mice given an LD50. Pathogenic mechanisms responsible for death may be different in these two groups of mice. Similarly the MCMV LD50 for B cell-deficient mice (treated with goat anti-mouse IgM serum) was 10-fold lower than the LD50 for mice treated with normal goat serum, but given an LD50 of virus, the latter died sooner after infection than the former. In contrast, there was little difference between the LD50 or time of death after MCMV infection of CBA x DBA F1 male mice (which are deficient in their response to thymic independent antigens) and their normal littermates, the CBA x DBA F1 female mice.

Topics: Animals; B-Lymphocytes; Cell Adhesion; Concanavalin A; Cytomegalovirus; Cytomegalovirus Infections; Female; In Vitro Techniques; Lectins; Lethal Dose 50; Lipopolysaccharides; Lymphocyte Activation; Male; Mice; Mice, Inbred BALB C; Mice, Inbred CBA; Mice, Inbred DBA; Mice, Nude; Mitogens; Spleen; T-Lymphocytes; Time Factors

Topics: Bone Marrow Examination; Candidiasis; Concanavalin A; Cytomegalovirus Infections; Fluorescent Antibody Technique; Histocompatibility Antigens; Humans; Hypersensitivity, Delayed; Immune Sera; Immunity, Maternally-Acquired; Immunoglobulins; Immunologic Deficiency Syndromes; Infant; Lectins; Lymph Nodes; Lymphocyte Activation; Male; Mitogens; Palatine Tonsil; Pedigree; Pneumonia, Pneumocystis; Thymidine; Tritium