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Easy to Use Fact SheetsThis area of our site is provided as a quick reference only. We strongly urge you to discuss medication concerns with your physician. Important Fact!
Entry Inhibitors work by interfering with HIV's entry into the CD4 cell. By interfering during the entry phase of the HIV life cycle, entry inhibitors block HIV replication.
Non-nucleoside reverse transcriptase inhibitors (NNRTIs) work by binding tightly to the enzyme reverse transcriptase which prevents viral RNA from converting to the viral DNA that infects healthy cells.
Like the nucleoside analogues such as Retrovir (AZT) and Videx EC (didanosine), nucleotide analogues inhibit reverse transcriptase. However, they are active in their native form, unlike nucleosides that only work in cells that have the machinery to activate the drug by a process called phosphorylation. This means that the nucleotide analogues may be active against HIV in a wider variety of infected cells.
Protease Inhibitors stop HIV replication by preventing the enzyme protease from cutting the virus into the shorter pieces that it needs to make copies of itself. Incomplete, defective copies are formed which can't infect cells.
Nucleoside Reverse Transcriptase Inhibitors (NRTIs) work by being incorporated into the viral DNA, making it ineffective. These compounds suppress replication of retroviruses by interfering with the reverse transcriptase enzyme. The nucleoside analogs cause premature termination of the proviral (viral precursor) DNA chain.
In an effort to improve medication adherence and to make it easier to take your medications each day, many medications are combined into one pill or capsule. Fewer pills each day has been shown to improve adherence which we know improves the effectiveness of HIV regimens. Updated: January 27, 2008 |
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