HIV Replication Process PDF

Summary

This document provides a detailed explanation of the HIV replication process, outlining the nine steps involved. It covers various inhibitors used to treat HIV infections, focusing on how they interfere with viral replication at different stages. The document is intended as a detailed, scientific overview and not for self-diagnosis or treatment recommendations.

Full Transcript

**Title: HIV Replication Process** **Step 1 Binding to cell membrane** **Entry Inhibitors:  ** - HIV binds to the receptors and co-receptors of CD4 cells, utilizing its gp120 protein to facilitate this attachment. Entry inhibitors block HIV\'s initial attachment and fusion with the host...

**Title: HIV Replication Process** **Step 1 Binding to cell membrane** **Entry Inhibitors:  ** - HIV binds to the receptors and co-receptors of CD4 cells, utilizing its gp120 protein to facilitate this attachment. Entry inhibitors block HIV\'s initial attachment and fusion with the host cell.  - CCR5 antagonists such as maraviroc (Selzentry) bind to the CCR5 co-receptor on CD4 cells, blocking CCR5-tropic HIV strains from binding and, therefore, entry into the cell.  **Step 2 Fusion** **Fusion Inhibitors:  ** - Fusion inhibitors can prevent the virus from merging with the cell membrane. These medications are reserved for treating HIV-1 that has become resistant to other ART medications.  - Fusion inhibitors like enfuvirtide (Fuzeon) work by attaching to the gp41 subunit of the virus, preventing the HIV envelope from merging with the CD4 cell membrane.  **Step 3 Reverse Transcriptase** **Reverse Transcriptase Inhibitors:  ** - Once inside the host cell, HIV employs reverse transcriptase to convert its RNA into DNA using reverse transcriptase. Reverse transcriptase inhibitors interrupt the conversion of viral RNA to DNA, effectively preventing the viral genetic material from being prepared for integration.  - Nucleoside/Nucleotide Reverse Transcriptase Inhibitors (NRTIs) mimic the natural building blocks of DNA, leading to the premature termination of the viral DNA strand. Examples include abacavir (Ziagen) and tenofovir (Viread).   - Nonnucleoside Reverse Transcriptase Inhibitors (NNRTIs) like efavirenz (Sustiva) directly inhibit the reverse transcriptase enzyme, preventing HIV DNA synthesis.  **Step 4 Integration** **Integrase Strand Inhibitors:  ** - Once formed, viral DNA travels to the host cell nucleus and integrates into the host\'s DNA with the help of integrase, a process blocked by integrase strand transfer inhibitors.   - Integrase Strand Transfer Inhibitors (INSTIs), such as raltegravir (Isentress) and elvitegravir (Vitekta), thwart the integration of viral DNA into the host genome by inhibiting the HIV integrase enzyme, a key step for the virus to replicate.  **Step 5 Transcription** **Step 6 and 7 Translation and viral assembly** **Step 8 Budding** **Protease Inhibitors: **  - After host DNA integration, the virus is transcribed, translated, assembled, and budded from the host cell. The new virus then must mature to become infectious, a process mediated by the HIV protease enzyme.   - Protease inhibitors block the protease enzyme, resulting in the release of non-infectious virus particles and hindering the virus\'s capacity to propagate and infect new cells. Examples include atazanavir (Reyataz) and darunavir (Prezista), which are often combined with other drugs like ritonavir to enhance their efficacy.  **Step 9 Viral release and maturation**

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