Of mice, monkeys and men

Article Abstract:

It has been difficult to find good animal models for infection with human immunodeficiency virus (HIV) and AIDS. Animal models are important in the study of the function of virus and to analyze strategies for prevention and treatment of infection. Studies involving animals would help answer some of the problems that are not understood with studies in cells grown in tissue culture. The importance of studies done in animal models is exemplified by studies with the viral gene nef. The protein encoded by nef is thought to regulate the production of the other genes of the virus. Studies in rhesus monkeys have shown that if monkeys are injected with a strain of virus that does not make the nef protein, the animals survive the viral injection. If monkeys are injected with the wild virus, they die. Thus, nef appears to be necessary for the complete disease spectrum to appear. Tissue culture studies with these two strains of virus did not show a significant difference in the replication of infected cells. Thus, the tissue culture results contradict the results that occur in vivo. Studies in animals have also helped to understand which portions of the envelope gene, which encodes the outer coat of the virus, are involved in the targeting of the virus to T lymphocytes and which portion of the virus is important in production of viral proteins. Another animal model that has been used is the SCID/hu mouse, in which the mouse's immune system is genetically deficient and is replaced with human immunological factors. The SCID/hu mouse can be used to determine the dose levels of certain anti-viral drugs and to test the effectiveness of vaccines against HIV and other therapeutic methods used to combat HIV infection. Chimpanzees are also used as an animal model for HIV infection and have been used to test the effectiveness of vaccines and other antiviral therapies. The use of animal models is imperative in the understanding of infection with the complicated HIV and to understand the viral and host factors that are involved in the disease state. (Consumer Summary produced by Reliance Medical Information, Inc.)

Models, HIV infection, HIV infections

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Tat protein of HIV-1 stimulates growth of cells derived from Kaposi's sarcoma lesions of AIDS patients

Article Abstract:

Patients with AIDS (acquired immunodeficiency syndrome), which is caused by infection with HIV-1 (human immunodeficiency virus type 1), often have Kaposi's sarcoma. Previous studies have shown that HIV-1-infected T cells secrete a factor which causes the growth of cells obtained from lesions of Kaposi's sarcoma. Animal model studies have shown that the tat gene, a gene involved in the regulation of HIV-1 growth, causes skin lesions similar to those seen in Kaposi's sarcoma. This study shows that the tat gene is released from cells that are infected with HIV-1, and from cells which have been experimentally given the tat gene. The tat gene product, the Tat protein, promotes the growth of cells derived from Kaposi's sarcoma lesions from patients with AIDS. Both recombinant Tat and Tat obtained from HIV, can stimulate growth. This growth is inhibited if the proteins are treated with antibodies against Tat, indicating an inhibition of Tat activity by antibodies. This inhibition of growth is seen both with cells that are infected with HIV-1, and with cells that have been bioengineered by the insertion of the gene encoding tat. Therefore, Tat can be released as an active protein, and is involved in the development and growth of Kaposi's sarcoma in HIV-1 infected patients. The inhibition of Tat activity, either by antibodies, as shown in this study, or by other mechanisms, may lead to a treatment for Kaposi's sarcoma. (Consumer Summary produced by Reliance Medical Information, Inc.)

Complications and side effects, Development and progression, Identification and classification, Growth factors, Kaposi's sarcoma

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HIV: to vaccinate or not to vaccinate?

Article Abstract:

Albert Sabin, a leading virologist, has expressed doubts about the possibility of making an effective vaccine against the human immunodeficiency virus (HIV). However, an immunological analysis shows that Sabin's arguments are faulty and do not justify delaying work on a vaccine. For instance, Sabin's assertion that HIV-infected cells do not express viral products at their surface overlooks the presence of major histocompatibility complex antigens at the cell surface that may overcome this obstacle to devising a vaccine.

Research, Column, AIDS vaccines, Sabin, Albert B.

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