Susceptibility to a mouse acquired immunodeficiency syndrome is influenced by theH-2

Hamelin-Bourassa, Diane; Skamene, Emil; Gervais, Francine

doi:10.1007/bf02421330

Cited by 34 publications

(20 citation statements)

References 35 publications

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“…The former elicited the disease after a significant delay of 18 weeks and even then some characteristic abnormalities did not reach their peak ex pression. Several authors have reported complex genetic control of the susceptibility of mice to infection with LP-BM5 MuLV [24][25][26]. Our unpublished results confirmed that certain strains arc totally resistant to the infection.…”

Section: Discussionsupporting

confidence: 79%

Blood Transfusion as a Means for Transmission of Retrovirus-Induced Lymphoproliferative Disease in Mice

Cunningham

Thacore

Zhou

et al. 1994

Int Arch Allergy Immunol

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Lymphoproliferative disease was elicited in C57BL/6KH and (BALB/c × C57BL/6)F1 hybrids by a single intraperitoneal injection of 10⁵ FFU of LP-BM5 virus preparation. The disease could reproducibly be transferred by a single intravenous transfusion of 0.2 ml of whole blood as well as 0.1 ml of blood cells, plasma or serum from the infected animals. F1 hybrids displayed a delayed development of the disease when an acellular virus preparation was administered, but they were fully susceptible to the disease when syngeneic blood from infected F1 donors was transfused. Blood from donors in the prodromal stage was as effective in transmission of the disease as blood from donors with fully developed disease. This indicated that in murine lymphoproliferative disease viremia develops very early in the course of the disease. It seems that using the blood transfusion one could develop a reliable semiquantitative assay for the infectiveness of the animals suffering from LP-MB5-induced lymphoproliferative disease.

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Section: Discussionsupporting

confidence: 79%

Blood Transfusion as a Means for Transmission of Retrovirus-Induced Lymphoproliferative Disease in Mice

Cunningham

Thacore

Zhou

et al. 1994

Int Arch Allergy Immunol

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“…C57BL/6 (B6) mice are highly susceptible to LP-BM5 MuLV (this represents a mixture of the replication-defective virus and the ecotropic helper virus) and develop MAIDS in several weeks after viral infection (17,18). We injected LP-BM5 MuLV intraperitoneally into B6 mice or B6 mice bearing the X chromosome-linked imm~odefidency (B6.x/d).…”

Section: Resultsmentioning

confidence: 99%

Delayed progression of a murine retrovirus-induced acquired immunodeficiency syndrome in X-linked immunodeficient mice.

Hitoshi

Okada

Sonoda

et al. 1993

The Journal of Experimental Medicine

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Stlmmal~The murine acquired immunodeficiency syndrome (MAIDS) caused by defective LP-BM5 murine leukemia virus (MuLV) is a disease that shows severe immunodeficiency with abnormal lymphoproliferation, and hypergammaglobulinemia in susceptible C57BL/6 (B6) mice. To examine the cellular mechanisms of development of MAIDS, we injected LP-BM5 MuLV intraperitoneaUy into B6 mice bearing the X chromosome-linked immunodefidency (xid). xid mice lack functionally mature B cells including Ly-1 B cells (also known as B-1 cells). All B6 mice died by 20 wk after LP-BM5 MuLV inoculation. In marked contrast, xid mice have continued to survive without any sign of MAIDS-related symptoms till at least 20 wk after the inoculation. The delayed progression of MAIDS in x/d mice appears to depend on xid mutation, according to our experiments using both sexes of (B6.xid x B6)F1 and (B6 x B6.xid)F1 mice. Furthermore, Ly-1 B cells, enriched by a FACS | were shown to integrate the defective genome and appeared to be a major virus-infected B cell population. Our data corroborate that Ly-1 B cells play an important role in the induction and progression of MAIDS.T he murine acquired immunodeficiency syndrome (MAIDS) 1 caused by a defective retrovirus (defective LP-BM5 murine leukemia virus [MuLV]) (1, 2), which encodes a gag fusion protein (Pr60S~s), is a disease that shows many similarities with human AIDS, in particular abnormal lymphoproliferation, polyclonal B cell activation, and severe immunodeficiency (3, 4). Previous studies have proven that complex cellular interactions between T and B cells are required for the induction and development of MAIDS. B cell abnormalities are shown in the presence of T cells of CD4 phenotype (5), whereas B cells are required for induction of phenotypic and functional T cell abnormalities in MAIDS (6). It is interesting that a recent study reported that the majority of cells infected with the defective LP-BM5 MuLV 1 Abbrrviations used in this paper: MAIDS, murine acquired immunodeficiency syndrome; MuLV, murine leukemia virus; xid, X-linked immunodeficiency.belongs to B cell lineages (7,8), implying that B cells trigger the induction and development of MAIDS. The development of hypergammaglobulinemia in MAIDS also suggests that B cell activation and its differentiation is associated with the induction of MAIDS.It still remains obscure, however, what kinds orB cell subsets are required for and involved in the induction and development of MAIDS. To examine these problems, we used the X-linked immunodeficient (xic 0 mice (9-12). The defects in x/d mice, which show the impaired humoral immune response to type II T cell independent antigens (9, 10, 12), has been implicated in the arrest of functional maturation of B cells. In particular, the lack of Ly-1 B cells (also known as B-1 cells [13]) is noticed in xid mice (11).Here we report that xid mice are resistant to MAIDS and Ly-1 B cells are a major virus-infected B cell population. Our data corroborate that Ly-1 B cells play an important role in the developme...

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“…In mice, genes within lhe H-2 complex influence the clearance of several retroviral [1][2][3], protozoan [4.5]. coccidian [6].…”

Section: Introductionmentioning

confidence: 99%

DistinctH-2complex control of mortality, and immune responses to tuberculosis infection in virgin and BCG-vaccinated mice

Апт

Авдиенко

Никоненко

et al. 1993

Clinical and Experimental Immunology

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SUMMARYWe have studied the impact of distinct haplotypes and of difTerent alleles at specific H-2 loci on: (i) the susceptibility to lethal form of experimental tubereulosis; (ii) the level of DTH to mycobaclerial antigens; (iii) the efficacy of vaccination wilh bacille Calmette-Gucrin (BCG); and (iv) the IgG production and Tcell proliferative response to H37Rv antigens. On lhe basis of median survival lime (MST) following primary inoculation wilh lethal dose of Myeobaeterium tutwrcidosis, susceptibility to infection associated with I-A'' and // alleles. host resistance associaled with /-/I* and D'' alleles. Mice bearing a disease-resistant phenotype also developed a vigorous DTH response. Vaccination with BCG before H37Rv infection significantly prolonged the .survival time of both resistant and susceptible animals, except in BIO.M (H-2') mice. The latter exhibited intermediate resistance to infection before but slight decrease in lhe MST following a high-dose BCG vaccination. Distinct H-2 regulation of su.sceptibility to lethal infection and of BCG vaccination efiicacy was confirmed in another relatively resistant //-^'-bearing strain A.CA,, in which mortality occurred more rapidly in vaccinated compared with primarily infected animals. The expression of the H-2' haplotype was associated wilh a low DTH response to tuberculin following vaccination and subsequent lethal infection. The lack of BCG protection against Myco. tubercutosis QhaWcnofi'uy BIO.M mice associated with the high titre of specific IgG, In addilion, these mice exhibited a unique ability to respond to65-kD aniigen by both IgG synthesis and T cell proliferation.

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Susceptibility to a mouse acquired immunodeficiency syndrome is influenced by theH-2

Cited by 34 publications

References 35 publications

Blood Transfusion as a Means for Transmission of Retrovirus-Induced Lymphoproliferative Disease in Mice

Blood Transfusion as a Means for Transmission of Retrovirus-Induced Lymphoproliferative Disease in Mice

Delayed progression of a murine retrovirus-induced acquired immunodeficiency syndrome in X-linked immunodeficient mice.

DistinctH-2complex control of mortality, and immune responses to tuberculosis infection in virgin and BCG-vaccinated mice

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