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Antiretroviral Drugs

 

HAART

 

     Like many other viruses, there are treatments to HIV that are able to allow the body to fight off HIV, or control its spread with certain limitations. Currently Highly Active Antiretroviral Therapy is used widely to treat for HIV, by using multiple classes of drugs to slow down the progression of HIV, while maintaining the patient in a more healthy state, from dying of opportunistic infections. Through the use of Highly Active Antiretroviral Therapy, patients are not cured from the virus but are significantly healthier than before, because HAART therapy slows down the growth of the virus and allows the patient to live with minimal side effects; depending on the combination and types of classes of drugs used.

 

Nucleoside Reverse Transcriptase Inhibitors

 

     Nucleoside Reverse Transcriptase Inhibitor (NRTI) also known as competitive inhibitors, is a class of antiretroviral drugs that are used to discourage the reverse transcription of viral RNA into cDNA, by allowing the reverse transcriptase to process the NRTI to create a strand of DNA with a few incorrect genetic blocks; which can not be further integrated to the infected host cell’s DNA. By sabotaging the process of viral RNA to cDNA, NRTIs does an effective job to prevent the virus to infect the host DNA, but are very dangerous, because unlike other treatments, NRTI is a basic building block to the reverse transcription of genetic material; so the major side effects of NRTI is that it interferes with mitochondrial DNA synthesis in other cells, which leads to high lactate, liver steatosis, myopathy, lipoatrophy, liver steatosis, and lactic acidosis.

Non-Nucleoside  Reverse Transcriptase Inhibitors

 

     Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTI) also known as noncompetitive inhibitors are a class of antiretroviral drugs that, block reverse transcription of viral RNA to cDNA, by binding to the viral transcriptase substrate; which disallows HIV to create its genetic material that would have infected the DNA of the infected host cell. NNRTIs are generally safe to many individuals, but certain individuals may be affected, because not all NNRTIs medications are created equally.

Integrase Inhibitors

 

     Integrase Inhibitors are also a class of antiretroviral drugs that are used to stop the production of HIV, by binding to the viral Integrase; which are enzymes that specifically bind the newly formed cDNA to the DNA of the infected host cell. By preventing the binding of the virus cDNA to the host DNA, the progression of HIV can be blocked significantly. Currently Integrase inhibitors pose no long term safety issues for the infected human being, and is considered the best antiretroviral treatment.

 

Protease Inhibitors

 

      Protease Inhibitors are a class of antiretroviral drugs that are used to stop the production of HIV, by binding to the viral protease; which are enzymes that specifically specifically cleave gag proteins to produce other important proteins gp41 and gp120 for the formation of the virion. By blocking the binding site of the viral protease, the virion structure for the virus would never form to allow the virus to leave the infected host cell. Although of its benefits, Protease Inhibitors do cause major side-effects, where if not monitored carefully and utilized in adjunction with ritonavir, will cause increased triglycerides, lipodystrophy, and increased risk of heart attack.

 

Entry Inhibitors

 

     Entry Inhibitors also known as fusion inhibitors are a class of antiretroviral drugs that are used to stop the binding of HIV to the host cell. Initially the HIV viruses infects a host cell by attaching to the gp120 surface of the CD4 receptor of the host cell, then exchanging a gp120 handshake between the host and the virus allows the virus to expose its gp41 surface, which is then used to bind to the surface and penetrate through the surface of the cell, and into the membrane of the host cell. With Entry Inhibitors, the process is blocked by interfering with either step of the fusion process for the HIV virion, by binding the the CCR5 receptor of the T-Cell. This prevents the entry for HIV, but is also dangerous when administered in great quantity because, although a great antiretroviral drug, may cause HIV tropism; which is where HIV adapts to utilize the alternative CXCR4 receptor of the host cell, creating a more potent virus.

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