Concerns raised about mouse models for AIDS
Article Abstract:
Researchers studying AIDS (acquired immunodeficiency syndrome) were exhilarated when it was discovered that the mouse could be used as a model for human HIV (human immunodeficiency virus) infection. Without an animal model it was difficult to study how the virus attacks the human immune system and to test drugs and vaccines. Mice with a genetic abnormality that inactivated their own immune systems were given transplants of cells from the human immune system; the action of the AIDS virus on human immune function was then studied in a type of 'living laboratory'. But scientists Paolo Lusso and colleagues report that using these mouse models for AIDS may yield misleading results and may also pose a health hazard. The potential problems stem from the chance that a common mouse virus will interact with the human AIDS virus, HIV-1, in the human immune cells that have been transplanted into the live mice. Because of this interaction, HIV-1 may gain the ability to replicate much faster and to infect new types of cells. Changes to HIV-1 have not yet been observed in the mouse model, but only in cultured cells outside of the animal. A risk to human health might occur if these same changes developed in live mice, because they might manufacture variant forms of HIV-1 which could be transmitted in new ways; one possible route of transmission could be through the air. The mice infected with HIV-1 are kept in controlled laboratories, and no alterations to HIV-1 have occurred. Another flaw in the mouse model is that any interaction between mouse viruses and human HIV could make HIV behave differently in mice than humans; this would make the mouse a biologically irrelevant, or useless, model of human disease. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: Science
Subject: Science and technology
ISSN: 0036-8075
Year: 1990
User Contributions:
Comment about this article or add new information about this topic:
Learning how to bottle the immune system
Article Abstract:
A new procedure has been developed by Richard Lerner of the Research Institute of Scripps Clinic to produce antibodies in bacteria instead of in mammalian cells. Antibodies, molecules which are normally made by the cells of the immune system, recognize foreign substances, or antigens, in the body. The current technology for growing monoclonal antibodies that are specific for one particular antigen is tedious, time consuming, and has a low probability of yielding an antibody with the desired specificity. The new technology involves the transfer of DNA, deoxyribose nucleic acid, which codes for the antibody-producing genes, into bacteria. The bacteria will produce a complete array of antibody molecules. The researchers will then have to isolate the particular antibody molecules they are interested in. Antibodies are normally produced according to information contained in two separate genes, which code for the two different chains that compose the antibody molecule. To produce a complete antibody molecule, the two genes must be present in the bacteria. This means that the two genes coding for the two chains must be joined together, then inserted into a virus as a vehicle to carry the genes into the bacteria. However, for some purposes, one chain of an antibody molecule may be sufficient to bind the antigen. Once the genes coding for the antibody molecule are isolated, changes can be made - for example, to make the antibody bind more tightly to the antigen. These procedures will revolutionize the way monoclonal antibodies are made and will extend the diversity and availability of monoclonal antibodies for use in diagnosis and therapy. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: Science
Subject: Science and technology
ISSN: 0036-8075
Year: 1989
User Contributions:
Comment about this article or add new information about this topic:
Cell communication failure leads to immune disorder
Article Abstract:
Five independent research teams have identified the gene defect that causes hyper-immunoglobulin M syndrome (HIM), an inherited immunodeficiency disease. The finding could lead to improved treatments for HIM and to the development of methods for blocking unwanted antibody production in autoimmune diseases.
Publication Name: Science
Subject: Science and technology
ISSN: 0036-8075
Year: 1993
User Contributions:
Comment about this article or add new information about this topic:
- Abstracts: Creep deformation and failure: effects of randomness and scatter. Multiaxial cyclic ratcheting in coiled tubing-- experimental program and model evaluation, part II
- Abstracts: Control damage of dental multilayers: Viscous deformation and fatigue mechanisms. Time model of rubber deformation
- Abstracts: Flipping the main switch in the central reward system? New populations of old add to poor nations' burdens. Street-wise crack research
- Abstracts: Retrovirus vectors: promise and reality. New startups move in as gene therapy goes commercial. Targeting retroviral integration
- Abstracts: Molecular biology lies down with the lamb. Chronic fatigue as chameleon