Effects of recombinant soluble CD4 (rCD4) on HIV-1 infection of monocyte/macrophages

Article Abstract:

The human immunodeficiency virus (HIV) binds to its cellular receptor, CD4. This binding is mediated by the viral surface glycoprotein gpl20, thus initiating viral infection at the cellular level. This process may also be partly responsible for the cytopathic properties of HIV. Regardless of the strain variations encountered within HIV and the differences between HIV-1 and HIV-2, CD4 binding is an essential part of the infectious process. Interruption of the binding process may be a means of altering infection. A soluble, cell-free form of the extracellular part of the CD4 molecule, known as rCD4, was previously shown to bind with HIV in a manner similar to the natural molecule. The bound rCD4 appeared, in earlier studies, to inhibit HIV infection of lymphoid cells. This study examines the effects of rCD4 on acute HIV infection of human pulmonary macrophages (PAM) and monocytes (monocytic U937 cells), and evaluates its ability to interfere with the possible transfer of infection to target lymphocytes. (Monocytes and lymphocytes are types of white blood cells.) The potential of the success of these effects is in the treatment of HIV infections such as AIDS. The rCD4 was capable of preventing infection of PAM cells at concentrations greater than or equal to 1 microgram per milliliter. The same concentration inhibited the transmission of HIV-1 to peripheral blood mononuclear leucocytes (PMNL) cultured together with chronically infected PAM in the absence of cell contact. With cell contact, rCD4 concentrations of 10 micrograms per milliliter produced substantial inhibition; transfer was completely blocked at higher concentrations. The potential value of rCD4 as a tool in the antiretrovirus efforts requires further study. (Consumer Summary produced by Reliance Medical Information, Inc.)

HIV (Viruses), HIV

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Combined treatment of symptomatic human immunodeficiency virus type 1 infection with native interferon-alpha and zidovudine

Article Abstract:

AIDS is caused by infection with the human immunodeficiency virus (HIV). Inhibition of HIV reproduction, specifically nucleic acid synthesis, with the use of zidovudine (AZT) therapy appears to be inadequate in treating chronic human immunodeficiency virus type 1 (HIV-1) disease. A preferred approach would utilize a combination of drugs to attack the cycle of virus reproduction at more than one target site. Previous studies indicate that the addition of interferon-alpha (IFN-alpha), which interferes with virus assembly and release, may be beneficial in this regard. Eighteen patients with active HIV infection were treated with the experimental regimen of AZT and IFN-alpha for a 12-week period. Success of the therapy was measured by a decrease in infectious virus levels or a decrease in p24 antigenemia (that is, a decrease in the blood level of the virus or a decrease in a protein in the envelope of the virus). Eight patients were given the full treatment schedule; six showed a positive response. Only one of the nine incompletely treated patients exhibited a significant decline in the virus level or antigenemia. IFN-alpha therapy resulted in significant side effects; several patients suffered fatigue and weight loss, and many were found to have decreased levels of hemoglobin, white blood cells and platelets. The extended treatment period required, high dosage, manner of administration, and debilitating side effects of IFN-alpha, in combination with AZT, does not seem to be a viable treatment modality. (Consumer Summary produced by Reliance Medical Information, Inc.)

Evaluation, Complications and side effects, Zidovudine, Interferon alpha

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