Inhibition of HIV replication by pokeweed antiviral protein targeted to CD4+ cells by monoclonal antibodies
Article Abstract:
The human immunodeficiency virus type 1 (HIV-1) binds to and enters the T lymphocytes of the helper subtype, through the CD4 molecule on the cell surface. This causes the destruction of these cells, which are necessary for the generation of an immune response; thus the end result is the immunodeficient state of AIDS. Agents which destroy the virus can be targeted to CD4+ cells, in order to prevent infection and destroy the virus in cells that already contain the virus. The replication of HIV-1 is inhibited by pokeweed antiviral protein in cells taken from infected patients that contain the virus. The protein is targeted to CD4+ cells by coupling it to a monoclonal antibody to CD4, CD5, or CD7 molecules expressed on CD4+ cells. The virus is inhibited from replicating at small concentrations of pokeweed antiviral protein and antibody. At these concentrations, the antibodies do not inhibit proliferation of normal CD4+ cells. The coupled antibodies were effective in inhibiting HIV-1 production for at least several weeks in cells from patients. Therefore, the use of pokeweed antiviral protein coupled to antibodies against components of helper T cells may be an effective treatment to prevent or inhibit HIV infection. Pokeweed antiviral protein also inhibits the replication of other viruses, and so this treatment may be useful against other viral diseases in humans. Studies are needed to test the effectiveness of the pokeweed antiviral protein coupled to antibodies in patients with HIV and other viral infections. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 1990
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The original sin of killer T cells
Article Abstract:
The cytotoxic T lymphocyte (CTL) response is asymmetrical in mice infected with strains of lymphocytic choriomeningitis virus (LCMV) that were either normal (wild type) or mutated at the immunodominant epitopes recognized by the CTL. The CTL responses from mice infected with the mutant virus cross-reacted equally with the mutant and wild-type strains. It is possible that helper T cells, primed by the original virus and subsequently stimulated by the new infection, activate memory B cells specific for the original virus. The response noted may also reflect the extremely strong CTL memory response to LCMV infection.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 1998
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Cellular immune responses to HIV
Article Abstract:
Issues are presented concerning the failure of the cellular immune response to completely control the infection caused by the human immunodeficiency virus. The role of CD4+ T-cells and CD8+ T-cells is discussed.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 2001
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