Zidovudine (AZT) reduces virus titer, retards immune dysfunction, and prolongs survival in the LP-BM5 murine induced immunodeficiency model

Article Abstract:

Very often, the efficient study of a disease involves the development of an animal model of that disease. In the case of AIDS, there are several animal models, but no single model is completely satisfactory. One model is the LP-BM5 mouse. Primary advantages of this model are its reproducibility in the laboratory, its cost-effectiveness, and the similarity of many of the observed defects to human AIDS. The major disadvantage is that the model is created using a combination of viruses, none of which is a lentivirus like HIV. The model employs murine leukemia virus, a variant of murine leukemia virus which causes focus formation in cultured mink cells, and a defective virus, which is actually responsible for the immune suppression. These viruses, which are genetically simpler than HIV and other lentiviruses, nevertheless create an immune deficiency syndrome in the infected mice which may be used to study virus-induced immunodeficiency. Investigators used this mouse model for the study of zidovudine, and have found that treatment with this drug increases survival of the mice. In addition, it was found that zidovudine reduced the immune dysfunction associated with disease progression. And, as is the case with human AIDS, zidovudine was not able to eradicate the viruses from the animal's system. However, it is not yet known whether this was due to the development of drug-resistant viruses, as occurs with the human immunodeficiency virus. (Consumer Summary produced by Reliance Medical Information, Inc.)

Research, Models, Retrovirus infections, Virus-induced immunosuppression

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Postexposure prophylaxis with zidovudine suppresses human immunodeficiency virus type 1 infection in SCID-hu mice in a time-dependent manner

Article Abstract:

Heath care employees risk exposure to the human immunodeficiency virus (HIV) as a result occupational mishaps, and chances appear to be high that exposure will result in eventual development of AIDS. Since the discovery that the drug AZT (zidovudine) may be an effective means by which to slow the progression from HIV seroconversion (development of antibodies to the infecting virus) to the development of full-blown AIDS, its usefulness for health care workers has been examined as well. Results thus far have been mixed, but in animals it has been shown that therapy with AZT is effective in modifying the course of infections similar to those caused by HIV. To determine whether or not therapy with AZT might suppress HIV infection in humans, SCID-hu mice, which are immunodeficient mice that have been surgically implanted with human lymph nodes, were injected with HIV and then treated with AZT at different times after infection. It was found that mice treated with AZT within two hours of infection showed no signs of infection after two weeks. Those treated between two hours and 36 hours later showed correspondingly less infection, and those treated after 48 hours showed no suppression in the replication of the virus two weeks after infection. This provides evidence that the time of treatment with AZT with respect to infection with HIV is a critical factor in the ability of AZT to suppress HIV replication. (Consumer Summary produced by Reliance Medical Information, Inc.)

Methods, Evaluation, Testing, Prevention, HIV (Viruses), HIV, Tests

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AZT demonstrates anti-HIV-1 activity in persistently infected cell lines: implications for combination chemotherapy and immunotherapy

Article Abstract:

AZT (3'-azido-3'-deoxythymidine; also known as zidovudine) is commonly used in the treatment of HIV infection. AZT prevents the synthesis of viral DNA and prevents HIV from infecting cells. AZT has been reported to be effective only in cells with acute HIV infection. However, interferon-alpha (IFN-a) has been reported to have anti-HIV activity in chronically infected cells. Since AZT is toxic and does not cure HIV, the development of more effective and less toxic treatments for HIV are needed. Therefore, the effectiveness of AZT and IFN-a in suppressing HIV infection was determined in cells that were grown in culture and transfected with HIV. An immunoassay was used that allowed the identification of cells that were making and releasing HIV. AZT suppressed acute HIV infection, an effect that increased with increasing drug concentrations. In contrast to previous studies, AZT prevented HIV production in chronically infected cells. The effects of IFN-a on acutely infected cells were variable, while chronic HIV infection was suppressed. The most effective therapy for suppressing HIV infection, both acute and chronic, was a combination of AZT and IFN-a. It is suggested that combination therapy be considered when designing clinical protocols for the treatment of HIV. (Consumer Summary produced by Reliance Medical Information, Inc.)

Interferon

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