HIV attacks the CD4 cells, which are specific types of white blood cells. This virus tends to change form as it multiplies in the body. When the mutation develops, it leads to drug-resistant strains of HIV. For a single drug therapy, the HIV medicines previously being administered and that controlled the person’s HIV becomes ineffective (Stirrup et al., 2020) . Treatment of HIV involves taking medications that slow the progression of the virus in the body. Since the virus is categorized as a retrovirus, antiretroviral drugs (ARV) are used in the treatment. These drugs are given with other ARVs, and this form of combination therapy is known as antiretroviral therapy (ART)
Before choosing the combination, specific considerations such as how many pills need to be taken, possible side effects, and interaction with each other and possible medication that may be considered.HIV medicines are grouped into seven classes of drugs, depending on how they fight the virus. They include inhibitors such as Fusion, INSTIs, PIs, NRTIs, NNRTIs, and post-attachment inhibitors, and CCR5 antagonists (Kemnic & Gulick, 2019) . The treatment begins by choosing an HIV regimen during antiretroviral therapy. This involves selecting three HIV medicines from at least two different classes (Kemnic & Gulick, 2019) . The first regime should include protease inhibitor boosted with cobicistat or ritonavir to increase its efficiency or a non-nucleoside reverse transcriptase, two NRTIs, and an NNRTI.
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HIV uses reverse transcriptase to convert RNA into DNA to infect the CD4 cells, and NNRTIs and NRTIs are effective in blocking the replication. It also requires a protease enzyme to replicate. The protease inhibitor blocks the enzyme's activity and thus prevents HIV from multiplying. The fusion inhibitor protects the CD4 cell from fusion with HIV by blocking any structural change that may lead to binding (Pagano et al., 2017) . This is quite similar to INSTIs, which blocks the active site of binding to the target DNA. HIV also attaches itself to CCR5 and CXCR4 to enter the human cell. The CCR5 antagonists block the CCR5 co-receptors while the post-attachment inhibitors bind the CD4 receptors, and both prevent the HIV from entering the cell.
References
Kemnic, T. R., & Gulick, P. G. (2019). HIV antiretroviral therapy. In StatPearls [Internet] . StatPearls Publishing.
Pagano, N., Teriete, P., Mattmann, M. E., Yang, L., Snyder, B. A., Cai, Z., & Cosford, N. D. (2017). An integrated chemical biology approach reveals the mechanism of action of HIV replication inhibitors. Bioorganic & medicinal chemistry , 25 (23), 6248-6265.
Stirrup, O. T., Asboe, D., Pozniak, A., Sabin, C. A., Gilson, R., Mackie, N. E., & Chadwick, D. (2020). Continuation of emtricitabine/lamivudine within combination antiretroviral therapy following the detection of the M184V/I HIV‐1 resistance mutation. HIV medicine .
