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Query: UMLS:C0021311 (Infection)
 38,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection with the Friend murine leukemia virus complex (F-MuLV) suppressed humoral antibody synthesis in vivo and lymphocyte mitogenesis in vitro. Both these effects of F-MuLV were under host genetic control. In vitro suppression of lymphocyte mitogenesis was regulated by a single autosomal gene called Fv-3 that is dominant for susceptibility. Genetic analyses, with the use of the susceptible DBA/2 and resistant B10.D2/n parents, their F1, intercross, and backcross progeny, indicated that a single autosomal gene dominant for susceptibility regulated the in vivo susceptibility to immunosuppression by F-MuLV. Individual [(DBA/2xB10.D2)F1xB10.D2] mice were typed both for susceptibility to F-MuLV-induced suppression of lymphocyte mitogenesis in vitro (an Fv-3 function) and susceptibility to immunosuppression by F-MuLV in vivo. Such an analysis indicated that the same mice that were susceptible or resistant to immunosuppression in vivo were susceptible or resistant to suppression of lymphocyte mitogenesis in vitro. Spearman's rank analysis of the data also indicated that the in vivo and in vitro immunosuppressive effects of F-MuLV were correlated with and not independent of each other. Thus Fv-3, which regulates the effect of F-MuLV on lymphocytes in vitro, also appears to regulate the effect of F-MuLV on antibody-forming cells in vivo.
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PMID:Mechanism of genetic resistance to Friend virus leukemia in mice. V. Relevance of Fv-3 gene in the regulation of in vivo immunosuppression. 10 Jun 4

Infection of Moloney mouse sarcoma virus (M-MSV) in adult mice of several inbred strains revealed that all strains except AKR are highly susceptible to M-MSV tumor development. F1 hybrids between AKR and CBA, DBA/2 or NIH mice are as resistant (93%) as the parental AKR strain, which indicates that resistance is transmitted as a dominant character. First backcross mice to the susceptible parent show a 3:1 ratio of resistant to susceptible mice. This is the expected ratio for two segregating loci which independently confer resistance. The incidence of resistant F2 mice is somewhat lower than expected. Further support for the two-gene hypothesis was obtained in second backcross mice. None of the major genes affecting MuLV infection (Fv-2 and H-2) seems to play any role in this system and no linkage was found with Thy. 1 and albino, dilute, agouti and brown markers.
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PMID:Genetic control of oncogenesis by murine sarcoma virus Moloney pseudotype. I. Genetics of resistance in AKR mice. 17 Feb 19

The kinetic study of immunosuppression caused by infection of mice with lymphocytic choriomeningitis virus WE (LCMV-WE) was assessed in DBA/2 (H-2d) and C57BL/6 (H-2b) mice. Infection with LCMV caused suppression of the Day 4 IgM response (complete in DBA/2 and incomplete in C57BL/6) and completely suppressed IgG responses on Days 9 and 42 to vesicular stomatitis virus (VSV) injected 2-11 days after LCMV. Suppression was partial when VSV was injected 16-28 days after LCMV-WE infection. The observed suppression between Day 2 and Day 11 was complete and nonspecific as revealed by the fact that these mice could not mount a secondary response to VSV when reinjected with the same VSV 42 days later. Nonspecificity of suppression was further indicated by the finding that the kinetics of recovery from suppression of the anti-VSV response were comparable for the VSV serotype used during the 2- to 11-day period after LCMV infection as for the serologically noncross-reactive second VSV serotype; both anti-VSV responses had recovered by Days 56-82 after LCMV infection. Once an anti-VSV antibody response was established, a subsequent LCMV-WE infection had no suppressive effect on Day 2 or Day 42 after a primary VSV infection. Also, the capacity of VSV-primed mice that were LCMV infected to respond to VSV in a secondary challenge infection with the same VSV was not impaired.
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PMID:Immunosuppression in mice by lymphocytic choriomeningitis virus infection: time dependence during primary and absence of effects on secondary antibody responses. 217 31

Virus-neutralizing monoclonal antibodies specific for 13 different genetically defined epitopes of glycoproteins gC, gB, and gD of herpes simplex virus type 1, strain KOS-321, were compared for their ability to provide passive immunity to DBA-2 mice challenged intracranially. Protection was highly specific, since individual monoclonal antibodies failed to protect against infection with monoclonal antibody-resistant (mar) mutants altered in the single epitope recognized by the injected antibody. The dose-response kinetics of passive immunity paralleled the in vitro neutralization titers for each antibody. No correlation was observed between immune protection and antibody isotype or complement-dependent in vitro neutralization titers. This suggests that virus neutralization was not the protective mechanism. In general, antibodies reactive with epitopes of gC were protective at the lowest antibody doses, antibodies specific for gB were less efficient in providing immunity, and antibodies against gD were the least effective. mar mutants with single epitope changes in gC and multiple epitope changes in gB showed highly reduced pathogenicity, requiring up to 5 X 10(6) PFU to kill 50% of infected animals. These findings indicated that antigenic variation affects virus growth and spread in the central nervous system. Thus, mutations which affect antigenic structure also can alter virus pathogenicity. The alteration of these epitopes does not, however, appreciably reduce the development of resistance to infection. Infection of mice with these mutants or inoculation of mice with UV-inactivated, mutant-infected cells before challenge rendered the animals resistant to infection with wild-type herpes simplex virus type 1.
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PMID:Passive immune protection by herpes simplex virus-specific monoclonal antibodies and monoclonal antibody-resistant mutants altered in pathogenicity. 241 19

The genetics of resistance to the Moscow strain of ectromelia virus was examined in crosses derived from resistant C57BL/6 (B6) and susceptible DBA/2 (D2) mice. Infection with 10(1) to 10(5) PFU of virus resulted in mortalities of 90 to 100% of D2, 0% of B6 and 0 to 3% of (B6 x D2) F1 mice by day 21. Among F1 x D2 backcross progeny, 49% of male and 18% of female mice died. Reciprocal backcrossing did not alter male or female mortality rates. These data are consistent with a single autosomal dominant gene controlling resistance to ectromelia in male mice and at least one additional dominant sex-limited gene controlling resistance in female mice. Fewer male F2 mice died than were predicted based on single-locus control and 32% of recombinant inbred (RI) strains derived from B6 and D2 progenitors expressed non-parental phenotypes. Therefore, additional resistance genes, not expressed in backcross mice, were apparently expressed in F2 mice and RI strains.
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PMID:Mousepox in inbred mice innately resistant or susceptible to lethal infection with ectromelia virus. V. Genetics of resistance to the Moscow strain. 280 4

Encephalomyocarditis (EMC) virus induction of diabetes mellitus in mice has proven to be an excellent experimental model for the pathogenesis of viral disease. In SJL and DBA/2 mice, diabetes results exclusively from the infection and damage of beta cells by the virus. In addition, in BALB/cBy mice subclinical beta cell damage caused by the virus is followed by autoimmune beta cell destruction, which results in hyperglycemia. Studies of two closely related plaque variants (EMC-D and EMC-B) selected from the M strain of EMC virus revealed differences in the interferon response associated with viral infection. The EMC-D variant causes diabetes in infected SJL mice by direct beta cell destruction. Infection with EMC-B does not cause diabetes and interferes with the production of diabetes by EMC-D due to the greater ability of EMC-B than of EMC-D to induce interferon in mice. Circulating interferon has a greater effect on inhibition of viral replication because local interferon production is amplified in interferon-primed cells infected with EMC-B. These properties are determined by the interferon-inducing particle (Ifp+) phenotype of EMC-B and the Ifp- phenotype of EMC-D.
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PMID:Encephalomyocarditis virus-induced diabetes mellitus in mice: model of viral pathogenesis. 282 21

Infection by the human immunodeficiency virus (HIV) induces T cell immunity in humans, chimpanzees and macaques. The protective value of this immune response is not clear. We have consequently developed a murine experimental system to study HIV-specific CD4 and CD8 T lymphocyte immunity in vitro and in vivo. BALB/c, DBA/2 and C3H/He mice were immunized with vaccinia virus (VV) recombinant VV-11.39 which expresses the gp160 glycoprotein of HIV-1. Primary and secondary cytotoxic T lymphocyte response to HIV were detected with histocompatible mouse target cells transfected with the HIV-1 env gene. Killer cells were positive for the Thy-1 and Ly-2 (CD8) T cell markers, and were restricted by class I H-2 histocompatibility antigens. Immunological memory specific for HIV-1 envelope antigens was clearly induced by vaccination with VV-11.39:spleen cells from mice vaccinated 4 weeks or more prior to assay generated CD4 and CD8 T lymphocyte responses following stimulation in vitro with HIV envelope antigens. The intensity of these responses increased with consecutive vaccinations, indicating that HIV-specific precursor T cell pools were progressively amplified. Finally, DBA/2 mice vaccinated with VV-11.39 developed protective immunity against a syngeneic tumor which expresses HIV-1 env antigens, leading to accelerated tumor rejection and increased survival.
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PMID:HIV-specific T lymphocyte immunity in mice immunized with a recombinant vaccinia virus. 290 93

Infection of mice with a temperature-sensitive mutant of Salmonella typhimurium C5TS allowed the survival of genetically susceptible mice. The ability to mount a delayed-type hypersensitivity (DTH) response to sheep erythrocytes during infection with C5TS was studied in various inbred mouse strains, recombinant inbred strains derived from C57BL/6 (susceptible) and A/J (resistant) mice, and C3H congenic mice. Suppression of the DTH response to sheep erythrocytes was found in mice that carried the Itys allele, the H-2b haplotype, or both. These genes are known to increase susceptibility to S. typhimurium infection. In contrast, no DTH response suppression was observed in mouse strains that carried other genes that increased susceptibility to S. typhimurium, e.g., DBA/2 and C3H/HeJ. Apart from a transient suppression in A/J mice, the DTH responses of resistant mice (A/J and CBA) were normal or increased. The DTH response to sheep erythrocytes could be restored in immunodepressed mice by increasing the immunizing dose, suggesting the possible role of activated macrophages in depression of the DTH response.
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PMID:Genetic control of Salmonella typhimurium-induced depression of delayed-type hypersensitivity to sheep erythrocytes in mice. 312 86

A recently described autoantibody-inducing agent in mice was further characterized. Tentatively designated AGIA (anti-Golgi apparatus-inducing agent), this agent has previously been shown to cause antibody production against Golgi apparatus (GA) antigen of cells from different vertebrate species as well as against tumour surface antigen of the Moloney murine sarcoma virus-non-producer transformant Sac. It was shown to possess the properties characteristic of lactate dehydrogenase-elevating virus (LDV). It induced elevation of lactate dehydrogenase levels in the blood, persistent lifelong viraemia in mice and serum titres of up to 10(11) infectious doses (ID50) per ml in the acute phase of infection. Its replication in vitro was limited to subpopulations of murine peritoneal macrophages. Electron microscopy of AGIA-infected macrophages and of serum of infected mice revealed virus-like particles with a morphology resembling LDV. The buoyant density of AGIA was approximately 1.14 g/ml. Both the enzyme-elevating activity and the autoantibody-inducing activity were shown to belong to LDV. Infection of STU mice with two established strains of LDV (LDVROW and LDVPLA) was also found to induce both autoantibody groups. In both cases, after infection with AGIA as well as after infection with the two known LDV isolates, anti-Sac cell antibodies occurred at comparable titres. However, anti-GA antibody titres were rather low after infection with LDVROW and LDVPLA compared with AGIA infection. Serological cross-reactivity was demonstrated between AGIA-, LDVROW- and LDVPLA-infected macrophages. AGIA induced anti-GA antibodies in all six mouse strains tested (STU, DBA/2, BALB/c, C3H/He, NMRI, C57BL/6); however, anti-Sac cell antibodies did not develop in C57BL/6 mice.
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PMID:Lactate dehydrogenase-elevating virus induces anti-Golgi apparatus antibodies. 359 63

Infection with the Isabel strain of Leishmania has been followed in several inbred strains of mice over an extended period. The mouse strains segregate into three major types with respect to susceptibility to infection: BALB/c, BALB.B and SWR/J are susceptible; DBA/1J is intermediate; and C57BL/6, C57BL/10, DBA/2J and B10.D2 are resistant. Infections with other leishmanial strains have been well-characterized in the BALB/c mice. Therefore, BALB/c mice were selected for extended studies. Progression of the disease was assessed by the following parameters: (1) numbers of parasites isolated from various tissues including footpad lesions, spleens, and lymph nodes and (2) the presence of metastatic lesions. This model should prove valuable in the study of the early immunological events in leishmaniasis.
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PMID:Experimental murine infection with the diffuse cutaneous leishmaniasis strain, Isabel. 367 47


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