New Approaches in HIV Management (Biochemistry)
November 24th 2008 12:28
Other Possible Approaches in Managing AIDS
At present, drugs that are designed to manage HIV are usually directed at either inhibiting reverse transcription of the virus (anti-retroviral) or inactivating certain protease enzyme that aids in manufacturing viral proteins to be incorporated to newly produced RNA of the virus in an infected cell (protease inhibitor). For so many years, these drugs have been the mainstay in delaying, if not totally stopping AIDS progression. But such use poses limitation. Literature would show that these drugs upon initial administration may significantly reduce viral load among patients. However later use has been observed to make the drugs ineffective (Devlin, 1996).
What are the possible reasons for the limitation of current drug therapies? The primary reason for this is drug resistance by continuously mutating HIV genes (especially those that dictate synthesis of viral proteins).
In the earlier part of the discourse, the life cycle and the mechanism of HIV replication have been discussed. It has emphasized that the hallmark of HIV replication is reverse transcription of the RNA virus to DNA by the enzyme reverse transcriptase. The DNA copy of the virus in turn, is being integrated into the host cell chromosomes. When the host cells become activated, the process of HIV reproduction then proceeds (Fauci and Lane).
At what point in the above process is contributory to producing drug-resistant, mutant genes? It is at the point of reverse transcription itself. In carrying out its action, reverse transcriptase does not perform proof-reading; thus its error rate is much higher than that of cellular DNA polymerase. And so if by chance reverse transcriptase errs in encoding one of the information from a parent HIV RNA into corresponding viral DNA, then what would be produced at the later stages would be mutants. It could have been nice if such mutants have shown decrease in their potency of infecting the body. Unfortunately, most mutants are as potent and as devastating as the original HIV. Even the viral proteins like the protease enzyme have shown mutations. And much worse, the effects of the drugs may not be reactive to such mutations.
Another reason for current drug limitation is the presence of immune cells that can act as reservoirs of HIV. These cells which serve as HIV reservoirs, usually are inactive CD$ cells (resting) containing provirus. In these cells HIV does not replicate. Current drugs cannot identify these cells. And by the time these resting cells become activated, HIV proceeds in duplicating, further aggravating an AIDS patient’s condition.
And so with such problems, other ways in managing AIDS are being cultivated, in hope of permanently controlling HIV infection. The succeeding portions discuss some of the developments in HIV treatment and management. All of which are still under serious scrutiny.
to be continued...
At present, drugs that are designed to manage HIV are usually directed at either inhibiting reverse transcription of the virus (anti-retroviral) or inactivating certain protease enzyme that aids in manufacturing viral proteins to be incorporated to newly produced RNA of the virus in an infected cell (protease inhibitor). For so many years, these drugs have been the mainstay in delaying, if not totally stopping AIDS progression. But such use poses limitation. Literature would show that these drugs upon initial administration may significantly reduce viral load among patients. However later use has been observed to make the drugs ineffective (Devlin, 1996).
What are the possible reasons for the limitation of current drug therapies? The primary reason for this is drug resistance by continuously mutating HIV genes (especially those that dictate synthesis of viral proteins).
In the earlier part of the discourse, the life cycle and the mechanism of HIV replication have been discussed. It has emphasized that the hallmark of HIV replication is reverse transcription of the RNA virus to DNA by the enzyme reverse transcriptase. The DNA copy of the virus in turn, is being integrated into the host cell chromosomes. When the host cells become activated, the process of HIV reproduction then proceeds (Fauci and Lane).
At what point in the above process is contributory to producing drug-resistant, mutant genes? It is at the point of reverse transcription itself. In carrying out its action, reverse transcriptase does not perform proof-reading; thus its error rate is much higher than that of cellular DNA polymerase. And so if by chance reverse transcriptase errs in encoding one of the information from a parent HIV RNA into corresponding viral DNA, then what would be produced at the later stages would be mutants. It could have been nice if such mutants have shown decrease in their potency of infecting the body. Unfortunately, most mutants are as potent and as devastating as the original HIV. Even the viral proteins like the protease enzyme have shown mutations. And much worse, the effects of the drugs may not be reactive to such mutations.
Another reason for current drug limitation is the presence of immune cells that can act as reservoirs of HIV. These cells which serve as HIV reservoirs, usually are inactive CD$ cells (resting) containing provirus. In these cells HIV does not replicate. Current drugs cannot identify these cells. And by the time these resting cells become activated, HIV proceeds in duplicating, further aggravating an AIDS patient’s condition.
And so with such problems, other ways in managing AIDS are being cultivated, in hope of permanently controlling HIV infection. The succeeding portions discuss some of the developments in HIV treatment and management. All of which are still under serious scrutiny.
to be continued...
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Comment by katyzzz
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Let's hope others respond to the indirect warning.