Literature DB >> 1658361

The majority of cells infected with the defective murine AIDS virus belong to the B-cell lineage.

M Huang1, C Simard, D G Kay, P Jolicoeur.   

Abstract

Murine AIDS (MAIDS) is caused by a defective retrovirus which encodes a gag fusion protein (Pr60gag). We previously reported that this virus induced an oligoclonal proliferation of infected cells and suggested that this cell expansion was an important event in the pathogenesis of MAIDS. To identify these target cells, we constructed novel defective viruses whose genomes could be detected with specific probes. Helper-free stocks of these viruses induced MAIDS. Using in situ hybridization and immunocytochemistry and Southern analysis, we found that most infected cells belong to the B-cell lineage. Transformation of these B cells appears to be the primary event responsible for the development of immunodeficiency. This animal model may be relevant to our understanding of AIDS, of the immunodeficiencies associated with B-cell lymphoproliferative disorders, and of the role of B-cell proliferation and transformation in the effects of superantigens, since Pr60gag appears to be a superantigen.

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Year:  1991        PMID: 1658361      PMCID: PMC250712     

Source DB:  PubMed          Journal:  J Virol        ISSN: 0022-538X            Impact factor:   5.103


  46 in total

Review 1.  T-cell responses to Mls and to bacterial proteins that mimic its behavior.

Authors:  C A Janeway; J Yagi; P J Conrad; M E Katz; B Jones; S Vroegop; S Buxser
Journal:  Immunol Rev       Date:  1989-02       Impact factor: 12.988

Review 2.  Immunologic tolerance: collaboration between antigen and lymphokines.

Authors:  G J Nossal
Journal:  Science       Date:  1989-07-14       Impact factor: 47.728

3.  Detection of specific sequences among DNA fragments separated by gel electrophoresis.

Authors:  E M Southern
Journal:  J Mol Biol       Date:  1975-11-05       Impact factor: 5.469

Review 4.  T-cell recognition of minor lymphocyte stimulating (Mls) gene products.

Authors:  R Abe; R J Hodes
Journal:  Annu Rev Immunol       Date:  1989       Impact factor: 28.527

Review 5.  Angioimmunoblastic lymphadenopathy: ten years' experience and state of current knowledge.

Authors:  H Knecht
Journal:  Semin Hematol       Date:  1989-07       Impact factor: 3.851

6.  A selective signaling defect in helper T cells induced by antigen-presenting cells from mice with murine acquired immunodeficiency syndrome.

Authors:  T Mizuochi; J Mizuguchi; T Uchida; K Ohnishi; M Nakanishi; Y Asano; T Kakiuchi; Y Fukushima; K Okuyama; H C Morse
Journal:  J Immunol       Date:  1990-01-01       Impact factor: 5.422

7.  Substitution of the U3 long terminal repeat region of the neurotropic Cas-Br-E retrovirus affects its disease-inducing potential.

Authors:  Y Paquette; D G Kay; E Rassart; Y Robitaille; P Jolicoeur
Journal:  J Virol       Date:  1990-08       Impact factor: 5.103

Review 8.  NIH conference. Angioimmunoblastic lymphadenopathy with dysproteinemia.

Authors:  A D Steinberg; M F Seldin; E S Jaffe; H R Smith; D M Klinman; A M Krieg; J Cossman
Journal:  Ann Intern Med       Date:  1988-04       Impact factor: 25.391

9.  Sequence analysis and acute pathogenicity of molecularly cloned SIVSMM-PBj14.

Authors:  S Dewhurst; J E Embretson; D C Anderson; J I Mullins; P N Fultz
Journal:  Nature       Date:  1990-06-14       Impact factor: 49.962

10.  B cells are required for induction of T cell abnormalities in a murine retrovirus-induced immunodeficiency syndrome.

Authors:  A Cerny; A W Hügin; R R Hardy; K Hayakawa; R M Zinkernagel; M Makino; H C Morse
Journal:  J Exp Med       Date:  1990-01-01       Impact factor: 14.307

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  36 in total

1.  Mice transgenic for a soluble form of murine cytotoxic T lymphocyte antigen 4 are refractory to murine acquired immune deficiency sydrome development.

Authors:  L De Leval; S Debrus; P Lane; J Boniver; M Moutschen
Journal:  Immunology       Date:  1999-12       Impact factor: 7.397

2.  Recovery from retrovirus-induced immune suppression in BDP/J mice: dominance of the "regressor' phenotype.

Authors:  G L Gilmore
Journal:  Immunology       Date:  1997-01       Impact factor: 7.397

Review 3.  Study of the T cell receptor repertoire in viral immunodeficiency disease.

Authors:  C Ciurli; R P Sékaly; H Soudeyns
Journal:  Springer Semin Immunopathol       Date:  1996

Review 4.  Superantigens related to B cell hyperplasia.

Authors:  N M Ponzio; V K Tsiagbe; G J Thorbecke
Journal:  Springer Semin Immunopathol       Date:  1996

5.  Murine AIDS is initiated in the lymph nodes draining the site of inoculation, and the infected B cells influence T cells located at distance, in noninfected organs.

Authors:  C Simard; M Huang; P Jolicoeur
Journal:  J Virol       Date:  1994-03       Impact factor: 5.103

6.  Antibody to the ligand for CD40 (gp39) inhibits murine AIDS-associated splenomegaly, hypergammaglobulinemia, and immunodeficiency in disease-susceptible C57BL/6 mice.

Authors:  K A Green; K M Crassi; J D Laman; A Schoneveld; R R Strawbridge; T M Foy; R J Noelle; W R Green
Journal:  J Virol       Date:  1996-04       Impact factor: 5.103

7.  ts1-Induced spongiform encephalomyelopathy: physical forms of high-mobility DNA in spinal cord tissues of paralyzed mice are products of premature termination of reverse transcription.

Authors:  P F Szurek; B R Brooks
Journal:  J Virol       Date:  1996-04       Impact factor: 5.103

8.  Adoptive transfer of polyclonal and cloned cytolytic T lymphocytes (CTL) specific for mouse AIDS-associated tumors is effective in preserving CTL responses: a measure of protection against LP-BM5 retrovirus-induced immunodeficiency.

Authors:  W R Green; K A Green; K M Crassi
Journal:  J Virol       Date:  1994-07       Impact factor: 5.103

9.  The MA (p15) and p12 regions of the gag gene are sufficient for the pathogenicity of the murine AIDS virus.

Authors:  J M Pozsgay; M W Beilharz; B D Wines; A D Hess; P M Pitha
Journal:  J Virol       Date:  1993-10       Impact factor: 5.103

10.  In murine AIDS, B cells are early targets of defective virus and are required for efficient infection and expression of defective virus in T cells and macrophages.

Authors:  W K Kim; Y Tang; J J Kenny; D L Longo; H C Morse
Journal:  J Virol       Date:  1994-10       Impact factor: 5.103

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