First, it injects itself into a Helper T cell; second, it slowly gets into the nucleus of the cell; thirdly, it integrates itself into the DNA in the nucleus of the cell causing a production of HIV proteins and lastly, the cells apoptosis occurs allowing the HIV virus the freedom to further infect other cells.
One leading way to stop or slow down the spread of the HIV virus is to inhibit its replication process. This means that drugs containing inhibitors such as reserve transcriptase inhibitors (RTIs) and protease inhibitors (PIs) are more likely to bind to the active site of the replicating HIV virus and stop it from spreading. RTIs have three Inhibitors that perform the function of stopping or inhibiting the replication the virus; but there are significant differences on the processes of how the inhibition occurs. II.
The three specific types of RTIs are: (1) Nucleoside Reverse Transcriptase Inhibitor (NRTIs): without a 3-hydroxy group. It goes into the viral DNA in order to stop the growth of the virus. (2) Non-Nucleoside Reverse Transcriptase Inhibitor (NNRTIs); it binds to the RT enzyme itself and stops it from moving. (3) Nucleotide Reverse Transcriptase Inhibitor (NtRTIs); works the same way as NRTIs but they already contain the phosphatase and do not need to undergo phosphorylation. Protease Inhibitors (PIs) on the other hand, are almost identical to the protein chain of which the protease enzyme binds; this makes it easy for PIs to bind to the Protease rendering the protein chain useless and nonfunctional. V However, although RTIs are one of the earliest and most recommended by the World Health Organization (WHO), protease inhibitors (PIs) have been studied and projected to work best with RTIs. .
Hypothesis.
If RTIs and PIs can be successful in inhibiting the replication of HIV-1/HIV-2 virus, then there will be significant decrease of infected cells and plausible increase in immune system function.
