Interferon decreases the growth inhibition of Mycobacterium avium-intracellulare complex by fresh human monocytes but not by culture-derived macrophages

Article Abstract:

Infection with the human immunodeficiency virus (HIV), which causes AIDS, may be complicated by infection with Mycobacterium avium-intracellulare complex (MAC). This microorganism is present in soil, water, house dust, and plants, and does not usually infect humans. MAC infection may develop when the microorganism has the opportunity to invade tissues, and in people who live in the southeastern United States, where MAC is prevalent. However, MAC infection is usually not persistent due to nonspecific resistance and specific immune mechanisms. Persistent MAC disease occurs under conditions of weakened immunity, such as AIDS. MAC infection in AIDS patients is characterized by the aggregation of bacteria-infected macrophages (a type of defense cell) in various tissues. The factors that influence the infectivity of MAC and the mechanisms for resistance against MAC infections were assessed. Monocytes (a type of white blood cell) of normal subjects were effective in killing a large proportion of MAC, whereas macrophages were less effective against MAC infection. The bactericidal effect of monocytes, or ability of monocytes to kill bacteria, was prevented by interferon-gamma (IFN-gamma), a protein with immune functions. MAC-infected cells exposed to IFN-gamma had higher levels of bacteria than those not treated with IFN-gamma. This suggests that IFN-gamma may activate the growth of MAC within the monocytes. However, IFN-gamma did not enhance MAC survival and growth in macrophages. IFN alpha/A2 had similar effects as IFN-gamma. These findings suggest that the ability of monocytes to kill mycobacteria is controlled by IFN. (Consumer Summary produced by Reliance Medical Information, Inc.)

Complications and side effects, Physiological aspects, AIDS (Disease), Monocytes, Interferon, Mycobacterial infections, Mycobacterium infections, Mycobacterium avium

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Inhibition of human immunodeficiency virus type 1 (HIV-1) replication by the dipyridodiazepinone BI-RG-587

Article Abstract:

The human immunodeficiency virus type 1 (HIV-1) causes AIDS. Cells in the human body replicate (multiply) by using DNA (the genetic material) to make RNA and proteins. However, HIV-1 replicates itself by a process called reverse transcription. This means that the virus uses an enzyme called reverse transcriptase (RT) to convert RNA into DNA. Drugs such as zidovudine (AZT), which is used to treat patients with HIV infection, prevent HIV-1 from replicating by inhibiting the RT enzyme. Although AZT has proven effective in treating some patients with HIV infection, newer drugs are needed because AZT-resistant strains of HIV-1 have developed and because of the side effects associated with long-term drug treatment. This article describes a study designed to test the antiviral activity of a new drug called BI-RG-587. This drug was designed to inhibit the RT enzyme and prevent replication of HIV-1. To test the antiviral activity of this drug, cells were infected with HIV-1 and grown in culture. Low doses of BI-RG-587 added to the culture were effective in preventing HIV-1 from replicating. BI-RG-587 and AZT were equally effective in preventing HIV-1 replication. BI-RG-587 did not prevent the HIV-1 virus from interacting with immune system cells called CD4+ lymphocytes, indicating that it does not prevent HIV-1 from reducing immune function. The results of this study indicate that BI-RG-587 exhibits antiviral activity against HIV-1 infection in a manner similar to AZT, by inhibiting the RT enzyme and viral replication. (Consumer Summary produced by Reliance Medical Information, Inc.)

HIV infection, Drug therapy, HIV infections, HIV (Viruses), HIV, Viruses

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