NRTIs are a class of anti-HIV drugs. When used in sequence with other anti-HIV drugs ?? usually three in total ??? this combination can block the spread of HIV in a person’s bloodstream. The first 3 NNRTIs listed above are currently approved by the US Food and Disease Control Center and can be used in similar combinations.
NNRTIs, sometimes referred to as “non-nucleoside analogs,” protect healthy T-cells in the body from contracting HIV.
When HIV infects a cell in a person’s body, it copies its genetic code into the DNA of the cell. This way, the cell is programmed ?? make new copies of HIV. The genetic material of HIV is in the form of RNA. To infect T cells, the necessity converts his RNA into DNA. This process requires the HIV reverse Transcriptase enzyme.
NNRTIs are hooked up? To convert Transcriptase and stop the enzyme from turning RNA to DNA. In this way, the genetic material of HIV cannot be fused with the healthy genetic material of the cell and prevents it from producing the new virus.
While non-nucleoside analogs (Viread is currently the only approved non-nucleoside analog) differ from nucleoside analogs, they act in much the same way. For nucleoside analogs to work, they must undergo some chemical changes (phosphorylation) to become active in the body. Non-nucleoside analogs skip this step if they have already been chemically activated.
What Are Protease Inhibitors (PIs)?
Protease inhibitors (PIs) are a type of anti HIV drugs (PrEP). When practiced in sequence with different anti HIV drugs ?? usually three in total ??? this combination can block the spread of HIV in a person’s bloodstream
Protease inhibitors prevent HIV infected T cells from producing new copies of the virus.
When HIV infects a cell in a person’s body, it copies its genetic code into the DNA of the cell. This way, the cell is programmed ?? make new copies of HIV. Once the genetic material of HIV (RNA) enters the DNA of a T cell, the cell produces a long strand of genetic material that must be separated and reassembled in a certain way to generate new copies of the virus. To separate this filament, a scissors-like enzyme called protease is required.
What are Incoming Inhibitors (including Fusion Inhibitors)?
Incoming inhibitors act to prevent HIV from entering healthy T cells in the body. They are different from most approved anti-HIV drugs?? protease inhibitors, nucleoside reverse transcrziptase inhibitors, and non-nucleoside reversed transcriptase inhibitors ?? who work against HIV after infecting the T-cell.
Incoming inhibitors act by attaching proteins to the surface of T cells or proteins to the surface of HIV. For HIV to bind to the T cell, proteins on the outer sheath of HIV must bind to proteins on the surface of the T cells. Incoming inhibitors prevent this from happening. Some take the GP 120 and GP 41 proteins on the surface of HIV. Others target the protein CD4 or CCR5 or CXCR4 receptors on the surface of the T cell. If incoming inhibitors are successful in blocking these proteins, HIV fails to bind to the T-cell surface and enter the cells.
Only one incoming inhibitor has been approved by the US Food and Drug Administration: Fuzeon ?? (T-20). This medicine aims at the gp41 protein on the surface of HIV. Some experimental drugs target the T-cell proteins: BMS-488043 targets the gp120 protein, PRO-542 the CD4 protein, and SCH-D the CCR5 protein.
HIV-positive people who have developed resistance to PI, NRTIs, and NRTIs may be able to benefit from incoming inhibitors as they represent a different class of medication. This is good news for HIV-positive people who have tried and failed many of the now approved anti-HIV drugs.