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At least 19 recordsLinked to original sources
PubMed1977

Immunoprophylaxis of experimental cytomegalovirus infection.

Experimental MCMV infection simulates human disease. Since human CMV has no experimental animal, the murine model is useful to study mechanism of immunity to CMV and immunoprophylaxis of CMV infection. The live attenuated MCMV, obtained by serial passages in MEF, was effective in immunization of mice against fatal MCMV infection. Every parameter of the MCMV infection was nullified by the prior immunization. The protective immunity was cell-mediated and independent of antibody production. The sensitized T lymphocyte interfered with virus replication in vitro and in vivo. Efficacy and possible risk of a human CMV vaccine were discussed with the murine model.

Animals↗
PubMed1975

Correlation of survival from murine cytomegalovirus infection with spleen cell responsiveness to Concanavallin A.

Spleen cells from nonlethally MCMV-infected weanling and adult DBA/2 mice had diminished responses to Con A stimulation. In contrast, only lethal MCMV infections were associated with a complete suppression of the Con A response. The immune response to SRBC was depressed even in asymptomatic infections of weanling and adult mice. A marked maturation of resistance to the lethal effects of MCMV infection was found to occur during the fourth week of life.

Age Factors↗
PubMed1979

Enhanced immune response late in primary cytomegalovirus infection of mice.

Murine cytomegalovirus (MCMV) infection has been previously shown to depress humoral and cell-mediated functions to non-MCMV antigens. In this report we show that in C3D2 mice undergoing nonlethal primary infection the depressed anti-sheep RBC plaque-forming cell (PFC) response is followed by an enhanced PFC response. Infected mice often generated twice the number of PFC per spleen than that of control mice. Total numbers of spleen cells as well as the recovery of virus from spleens of infected mice did not distinguish the depressed from the enhanced phase of the response. Investigation of the kinetics of the response revealed a defect in shutdown regulation. This enhanced PFC response during primary MCMV infection was not reflected in measurements of serum hemagglutinin. These findings suggest that MCMV induces an impairment of immunoregulation.

Animals↗
PubMed2026

Clonal stochasticity in early NK cell response to mouse cytomegalovirus is generated by mature subsets of varying proliferative ability.

Natural killer (NK) cells are classically defined as innate immune cells, but experiments show that mouse cytomegalovirus (MCMV) infection in C57BL/6 mice can cause NK cells to undergo antigen-specific proliferation and memory formation, similar to adaptive CD8+ T cells. One shared behavior between CD8+ T cells and NK cells is clonal expansion, where a single stimulated cell proliferates rapidly to form a diverse population of cells. For example, clones derived from single cells are most abundant during expansion when they are primarily CD27- for NK cells and CD62L- for T cells, phenotypes derived from precursor CD27+ and CD62L + cells, respectively. Here we determined the mechanistic rules involving proliferation, cell death, and differentiation of endogenous and adoptively transferred NK cells in the expansion phase of the response to MCMV infection. We found that the interplay between cell proliferation and cell death of mature CD27- NK cells and a highly proliferative CD27-Ly6C- mature subtype and intrinsic stochastic fluctuations in these processes play key roles in regulating the heterogeneity and population of the NK cell subtypes. Furthermore, we estimate rates for maturation of endogenous NK cells in homeostasis and in MCMV infection and found that only NK cell growth rates, and not differentiation rates, are appreciably increased by MCMV. Taken together, these results quantify the differences between the kinetics of NK cell antigen-specific expansion from that of CD8+T cells and unique mechanisms that give rise to the observed heterogeneity in NK cell clones generated from single NK cells in the expansion phase.

Animals↗
PubMed1979

Development in vitro of cytotoxic lymphocytes against murine cytomegalovirus.

Lymphocytes cytotoxic for mouse embryo fibroblasts (MEF) infected with murine cytomegalovirus (MCMV) were produced by in vitro culture of "memory" spleen cells with UV-irradiated, MCMV-infected, MEF. Cytotoxic lymphocytes were developed from spleen cells of mice 10 to 240 days after infection with MCMV. The cytotoxic cells carried the theta and Ly 2 antigens, and were H-2 restricted in the recognition of infected target cells.

Animals↗
PubMed1978

Murine model for immunoprophylaxis of cytomegalovirus infection. I. Efficacy of immunization.

Murine cytomegalovirus was utilized as a model for human cytomegalovirus, which had no experimental animal, to study immunoprophylaxis of the cytomegalovirus infections. (1) Murine cytomegalovirus (MCMV) serially propagated in mouse embryonic fibroblasts had lost pathogenicity for weanling mice including neonatally thymectomized mice. (2) The cell culture-adapted MCMV was effective as a "live, attenuated virus vaccine" against challenge by virulent, mouse-passaged MCMV. (3) The immunization via intraperitoneal route protected mice from every parameter of MCMV infection. These included clinical signs, virus replication, histopathology and mortality. (4) The protective immunity was active against the virulent MCMV which was not neutralized by the rabbit anti-attenuated MCMV serum.

Animals↗
PubMed1979

Replication of murine cytomegalovirus in murine Y-1 cells.

Murine Y-1 cells, a continuous epithelial cell line derived from an adrenal adenocarcinoma, are highly susceptible to murine cytomegalovirus (MCMV) infection. Inoculation of these cells with MCMV results in production of infectious virus and is associated with development of both cytopathic changes and the expression of viral-specific nuclear and cytoplasmic antigens. Examination of the ultrastructure of infected Y-1 cells reveals MCMV in various stages of replication. Cytomegalovirus replication in this hormone-responsive epithelial cell line should provide a model system in which virus--host cell interactions and their effects on cellular metabolism can be studied.

Adenocarcinoma↗
PubMed1976

Effect of murine cytomegalovirus on the in vitro responses of T and B cells to mitogens.

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.

Animals↗
PubMed1979

Latent cytomegalovirus infection of BALB/c mouse spleens detected by an explant culture technique.

Latent murine cytomegalovirus (MCMV) infection of BALB/c mouse spleens was studied using several methods including an explant tissue culture technique, co-cultivation on allogeneic and syngeneic cell cultures and nucleic acid hybridization. BALB/c mice experience latent infection which persists for at least 6 months and involves only a small fraction of spleen cells. The explant culture technique proved to be much more sensitive than other methods for detecting latent infection of lymphoid tissues.

Animals↗
PubMed1979

Age-related neurocytotropism of mouse cytomegalovirus in explanted trigeminal ganglions.

Human cytomegalovirus (CMV) causes severe congenital neurologic disease; adult neural infection is associated with transient cranial nerve palsies. In our experimental model, mouse CMV (MCMV) infects neurons and Schwann and satellite cells of cranial nerve ganglions. To study the fate of MCMV in nerve tissue, we explanted trigeminal ganglions from newborn, suckling, and weanling mice, 3 to 36 days after intracranial inoculation. Negative explants were co-cultivated with mouse embryo tissue culture (METC) to test for latency. MCMV, identified by electron microscopy, replicated in fibroblasts, Schwann cells, and/or satellite cells and neurons of trigeminal explants from newborn and suckling, but not weanling, mice. No latent virus was detected by our methods. The age differences in viral replication may be due to the age-dependent intrinsic cellular mechanisms and host inflammatory and immunologic response. Though neurons are infected, they remain relatively resistant to CMV replication.

Age Factors↗
PubMed1979

Activation of reticuloendothelial cells following infection with murine cytomegalovirus.

Macrophage and reticuloendothelial system function was investigated in adult, female C3H mice during the course of a nonlethal infection with murine cytomegalovirus (MCMV). Peritoneal macrophages harvested from mice infected three to 21 days previously were tumoricidal in vitro for a syngeneic mammary tumor cell line and showed antiviral activity by suppressing replication of vaccinia virus in a fibroblast monolayer. In addition, macrophages harvested from animals on days 7 and 14 after MCMV infection manifested augmented phagocytosis of yeast particles in vitro. Furthermore, enhanced levels of chemiluminescence were emitted during phagocytosis of zymosan particles by macrophages harvested on days 3 and 7 after MCMV infection. Finally, enhanced protection against Listeria monocytogenes was demonstrated in mice on days 7, 14, and 21 after MCMV infection. These findings support the concept of activation of the reticuloendothelial system during viral infection.

Animals↗
PubMed1976

Synergistic effect on mortality in mice with murine cytomegalovirus and Pseudomonas aeruginosa, Staphylococcus aureus, or Candida albicans infections.

A synergistic effect on mortality was demonstrated in a combined infection of mice with murine cytomegalovirus (MCMV) and Pseudomonas aeruginosa, Staphylococcus aureus, or Candida albicans. Mice infected intraperitoneally with a 0 to 20% lethal dose inoculum of MCMV 3 days prior to the intravenous injection of a 0 to 20% lethal dose inoculum of either the bacteria or fungus demonstrated a striking enhancement of mortality. MCMV-infected mice given Pseudomonas or Staphylococcus exhibited a 90 to 100% mortality within 24 to 48 h, whereas 80% of viral-infected animals injected with Candida died in 5 days. Injection of the bacteria or fungus at various times during the MCMV infection resulted in enhanced mortality on days 0,1,2, and 3 of the viral infection. Greatest synergism was observed on day 3, with a progressive decline in death rates thereafter. Immunization with MCMV abrogated the synergistic effect on mortality in all three combined infections. Immunization with Pseudomonas reduced mortality in the combined MCMV-Pseudomonas infection. These results indicate that mice exhibit a markedly enhanced susceptibility to bacterial and fungal infections during the course of the MCMV infection and suggest that the enhancement may be related to viral-induced alterations in host resistance.

Animals↗
PubMed1977

Alteration of host defense mechanisms by murine cytomegalovirus infection.

An animal model of a sublethal infection, utilizing murine cytomegalovirus (MCMV), was developed to determine whether immunological factors could contribute to the establishment of a persistent viral infection. Adult female C3H mice inoculated intraperitoneally with 10(5) plaque-forming units of MCMV developed splenomegaly 5 to 12 days after infection. Virus replicated to peak titers (10(3) to 10(6) plaque-forming units per g of tissue) in liver, spleen, lung, kidney, and salivary gland tissue during the acute phase of the infection (3 to 12 days); it then decreased to undetectable levels in all tissues except salivary gland. Serum interferon was detected as early as 12 h after infection, peaked at 36 h (1,093 U/ml), and was undetectable by 4 days after infection. MCMV-infected animals were hyporeactive to interferon induction with New castle disease virus on days 5 to 9 of the infection. Splenic lymphocyte reactivity to phytohemagglutinin and lipopolysaccharide was normal early during the course of the infection, was suppressed during the acute phase of the infection, and had returned to normal by day 18. These data indicate that several parameters of host defense are transiently suppressed during the course of a MCMV infection. The capacity of cytomegaloviruses to alter host resistance may be one factor that contributes to the establishment of a persistent infection.

Animals↗
PubMed1978

Effects of macrophages in resistance to murine cytomegalovirus infection.

In a preliminary experiment, the protective effects of peritoneal macrophages was shown by transferring macrophages from adult mice to newborn and to 7 and 14 days old mice. It was demonstrated that such transplantation protect suckling mice from intraperitoneal infection with MCMV by reducing the mortality rate from 100% to 27%.

Animals↗
PubMed1977

Role of T lymphocytes in recovery from murine cytomegalovirus infection.

Congenitally athymic nude (Nu/Nu) mice inoculated intraperitoneally with murine cytomegalovirus (MCMV), in doses as low as 1.3 X 10(1) plaque-forming units succumbed to the infection. In contrast, the mean lethal dose for heteroxygous euthymic (Nu/+) littermates was 4 X 10(3) plaque-forming units. Though histopathological changes consistent with MCMV infection were found in the spleen, lungs, and adrenals of nude mice, there were only small focal areas of involvement in the liver. In contrast, Nu/+ mice dying from infection had pathological evidence of severe hepatitis. Spleen cells from immune and control BALB/c mice were injected intravenously into syngeneic mice that had been inoculated previously with lethal doses of MCMV intraperitoneally. Mice receiving 1 X 10(7) or more immune spleen cells were protected against the infection, whereas mice receiving 1 X 10(8) control spleen cells or immune serum were not. Treatment of immune spleen cells with anti-theta serum and complement significantly reduced their protective effect. Immune mechanisms associated with T lymphocytes appear to be critical for recovery from MCMV infection.

Animals↗
PubMed1975

Pathogenesis of of cytomegalovirus infection. I. Activation of virus from bone marrow-derived lymphocytes by in vitro allogenic reaction.

After infection in utero or at birth with a cell culture adapted strain of mouse cytomegalovirus (MCMV), several mouse strains developed a latent virus infection in the presence of specific antiviral antibodies. Up to 5 mo after infection, MCMV could be activated and recovered from spleen lymphocytes of the infected animals that were co-cultivated with histoincompatible (H-2 foreign) mouse embryo cells from uninfected animals. In contrast, co-cultivation of lymphoid cells from infected mice with mouse embryo cells from syngeneic, histocompatible (H-2 similar) donors did not activate MCMV. Similarly, MCMV was not recovered from sonicated lymphoid cells. Virus was activated by treating viable lymphoid cells with lipopolysaccharide, a B-cell mitogen, but was not activated by a variety of other mitogens such as phytohemagglutinin, concanavalin A, or pokeweed mitogen. Subsequent purification of lymphoid cells from the infected mice by a variety of techniques indicated that MCMV was harbored in the B-lymphocyte population.

Animals↗
PubMed1978

Effect of concurrent cytomegaloviral infection and undernutrition on the growth and immune response of mice.

Mice were inoculated with murine cytomegalovirus (MCMV) passaged in cell cultures within 24 h of birth and subsequently fed an adequate or a low-protein diet after weaning; increases in body weight, the blastogenic response of lymphocytes to T and B cell mitogens, and the capability to produce antibodies to T or B cell-dependent antigens were observed for the first 28 to 42 days of life. Neonatal infection resulted in immunosuppression and retarded physical growth through the first 4 weeks of life. After weaning (3 weeks), the effect of MCMV infection of well-nourished mice paralleled the effect of undernutrition in uninfected animals. Undernutrition and MCMV infection functioned synergistically.

Animals↗