Antiviral agents with activity against human retroviruses

Article Abstract:

Antiviral agents which are known to have activity against the human immunodeficiency virus type 1 (HIV-1) were tested for activity against several human retroviruses: four strains of HIV-1; one strain of HIV-2 (a type of HIV that was isolated from patients with AIDS in northwest Africa); and a strain of human T-cell lymphotropic virus type I (HTLV-I), which causes adult T cell leukemia. The effects of the antivirals were measured in terms of their inhibition of viral infectivity when the virus was free (outside of a cell), and by a cell-to-cell infection system involving the inhibition of a cell fusion reaction. The antivirals tested were two sulfated polysaccharides, lentinan sulfate and dextran sulfate; a nonsulfated polysaccharide PSK; E-P-LEM (a polysaccharide produced by the fungus Lentius edodes); glycyrrhizin sulfate; and two nucleoside analogues, AZT (zidovudine) and DHT (didehydro-dideoxythymidine). All the substances tested inhibited the infectivity of the free HIV-1 and HIV-2 viruses. No cell-free system for testing HTLV-I infectivity exists at present. Cell-to-cell infection by HIV-1, HIV-2 and HTLV-I was inhibited only by the polysaccharides, E-P-LEM and glycyrrhizin sulfate, and not by the nucleoside analogues. This was as expected since the nucleoside analogues do not interfere with the binding of the proteins of the virus to the receptor on the cell surface, while polysaccharides do. The degree of inhibition of the fusion reaction varied among the strains of HIV-1. Understanding the effectiveness of various antivirals against the different types of disease-causing human retroviruses is important to maximize the effectiveness of treating patients with these drugs. (Consumer Summary produced by Reliance Medical Information, Inc.)

HIV (Viruses), HIV, Nucleosides, HTLV (Viruses), HTLV viruses, Virus inhibitors

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Sulfated polysaccharides as potent inhibitors of HIV-induced syncytium formation: a new strategy towards AIDS chemotherapy

Article Abstract:

The human immunodeficiency virus type 1 (HIV-1) infects CD4+ cells, which are a type of immune cells. The replication or multiplication of the virus within the cells eventually results in the destruction of the CD4+ cell. The CD4+ cells that survive HIV-1 infection form a protein called glycoprotein gp120 on their surface, which interacts with uninfected CD4+ cells. This interaction then results in the formation of giant cells that have several nuclei and are called a syncytium. The formation of a syncytium may be involved in the depletion of CD4+ cells in patients with acquired immunodeficiency syndrome (AIDS). This study showed that the interaction between HIV-infected cells and uninfected cells results in the destruction of the uninfected cells. Sulfated polysaccharides, which prevent viral replication, were shown to prevent cell fusion or merging, and thereby protect the uninfected CD4+ cells against destruction by killer HIV-1-infected cells. Azidothymidine, a drug used to treat HIV infection and AIDS, has no effect on the fusion process. If the interaction between infected and uninfected CD4+ cells is a crucial step in the disease process of AIDS, agents that interfere with the fusion process may be useful in treating AIDS. (Consumer Summary produced by Reliance Medical Information, Inc.)

Physiological aspects, Drug therapy, T cells

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Prevention of murine AIDS development by (R)-9-(2-phosphonylmethoxypropyl)adenine

Article Abstract:

A new antiviral agent seems to be effective in preventing HIV from reproducing. Researchers tested (R)-9-(2-phosphonylmethoxypropyl)adenine (PMPA) and 9-(2-phosphonylmethoxyethyl)adenine (PMEA) on mice infected with the murine leukemia virus. This virus causes a mouse form of AIDS called MAIDS. Both PMPA and PMEA initially seemed effective in preventing MAIDS in these mice. However, all of the mice who received PMEA eventually developed MAIDS, whereas only one mouse who received PMPA developed MAIDS.

Research, AIDS research

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