Basic approaches to anti-retroviral treatment

Article Abstract:

The replication of the human immunodeficiency virus (HIV, which causes AIDS) can be divided into two phases, an early and late phase. The early phase includes the following steps: the virus binds to the host cell; the membranes of the virus and cell fuse together; the genetic material of the virus leaves the structural unit of the virus; and the viral genetic material is converted to a type that is similar to that of the host cell. Compounds that inhibit the early stage of HIV infection prevent the virus from entering and infecting new cells. This group of compounds consists of agents that block the virus from adsorbing onto cells, and those that prevent the conversion of the genetic material of the virus into a type similar to that of the host. The latter group includes zidovudine, DDC (2',3'-dideoxycytidine) and DDI (2',3'-dideoxyinosine). These molecules inhibit reverse transcriptase, a central enzyme in the conversion process. The late phase of HIV replication involves the translation of the genetic material into new proteins which are made into new viral particles capable of infecting other cells. Compounds that inhibit the late stage of infection block the formation of new viruses, and thereby prevent more cells from being infected. Such compounds include antisense oligodeoxynucleotides, or nucleotides with a genetic composition similar to that of the virus. These agents bind to the viral genetic material, and then block further activity. Other compounds that impede the late stage of infection include agents that inhibit the cleavage of proteins and those that block glycosylation (the addition of sugar molecules to the proteins). These inhibitors prevent precursor proteins from being processed into mature and functional proteins, and thus inhibit the formation of mature virus. To provide more effective treatment in preventing the replication of HIV, various agents may be used together, particularly those that inhibit the early phase and the late phase. Combined treatment would inhibit HIV replication in cells that have already been infected and prevent infection of new cells. (Consumer Summary produced by Reliance Medical Information, Inc.)

Drug therapy, HIV (Viruses), HIV, Genetic aspects, Viruses, AIDS (Disease)

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Impeded progression of Friend disease in mice by an inhibitor of retroviral proteases

Article Abstract:

The protease inhibitor KH164 blocked the replication of human immunodeficiency virus type 1 (HIV-1) in a laboratory study of human T4 cells and inhibited progression of Friend disease in virally-infected mice. HIV-1 protease, an enzyme, plays an essential role in the development of virus particles. In the first phase of the study, two protease inhibitors, KH161 and KH164, were found to inhibit HIV-1 replication in acutely infected cells even more effectively than the drug zidovudine (ZDV), which currently used to treat HIV infection. Unlike ZDV, however, both KH161 and KH164 were also able to block virus production in chronically-infected cells. In phase two, researchers compared the response to KH161 and KH164 in normal mice and in mice infected with Friend virus complex, which replicates similarly to HIV-1. One of the protease inhibitors, KH164, blocked progression of Friend disease in the infected mice almost as effectively as ZDV. These findings suggest protease inhibitors may block virus production in humans as well.

Research, Evaluation, HIV infection, HIV infections, Protease inhibitors

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