"Figure 9.10: Antiretroviral therapy (ART) is typically used for the treatment of HIV. The targets of drug classes currently in use are shown here. Figure description available at the end of the chapter. Targeted therapy for HIV Fusion/entry inhibitors are a class of drugs employed in HIV treatment that specifically target the initial stages of the virus life cycle blocking the fusion of HIV with the host cell membrane preventing viral entry into host cells (figure 9.11). Non-nucleoside reverse transcriptase inhibitors (NNRTIs) are a class of antiretroviral drugs used in the treatment of HIV. They work by binding to the viral enzyme reverse transcriptase, disrupting its function, preventing the conversion of viral RNA into DNA, thereby hindering the replication of the virus. Nucleoside reverse transcriptase inhibitors (NRTIs) act by mimicking the building blocks of DNA. Once incorporated into the growing viral DNA chain, NRTIs terminate the process, preventing further replication and inhibiting the progression of HIV infection. Integrase inhibitors are a class of antiretroviral drugs that specifically target the viral enzyme integrase. By blocking the integration of viral DNA into the host cell genome, these inhibitors disrupt the virus’s ability to establish a permanent infection, ultimately suppressing HIV replication.\n\nFigure 9.11: Targeting HIV replication. Figure description available at the end of the chapter. Protease inhibitors are designed to block the activity of the viral enzyme protease. By inhibiting protease, these drugs prevent the maturation of newly formed viral particles, ultimately curtailing the production of infectious HIV and slowing the progression of the disease. Targeted therapy for Hepatitis C Glecaprevir and pibrentasvir (Mavyret®) are antiviral drugs used in combination for the treatment of chronic hepatitis C infections. Glecaprevir is an NS3/4A protease inhibitor, while pibrentasvir is an NS5A inhibitor. Together, they work synergistically to disrupt the viral life cycle, inhibiting viral replication and assembly. The mechanism of action involves glecaprevir inhibiting the NS3/4A protease, a key enzyme in the viral polyprotein processing, and pibrentasvir targeting the NS5A protein, crucial for viral RNA replication and assembly. This dual mechanism results in a high barrier to resistance and improved efficacy against a broad range of hepatitis C virus genotypes. Common adverse effects of the glecaprevir/pibrentasvir combination therapy include fatigue, headache, and nausea.\n\nMechanism of Action | Drug | Clinical Uses\n\nNucleoside analog inhibition of nucleic acid synthesis | Acyclovir | Herpes virus infections\n\nNucleoside analog inhibition of nucleic acid synthesis | zidovudine | HIV infections\n\nNucleoside analog inhibition of nucleic acid synthesis | Ribavirin | Hepatitis C virus and respiratory syncytial virus infections\n\nNon-nucleoside noncompetitive inhibition | Etravirine | HIV infections\n\nInhibit escape of virus from endosomes | Amantadine, rimantadine | Infections with influenza virus\n\nInhibit neuraminidase | Oseltamivir, zanamivir | Infections with influenza virus\n\nInhibition of protease | Ritonavir | HIV infections\n\nInhibition of integrase | Raltegravir | HIV infections\n\nInhibition of membrane fusion | Enfuvirtide | HIV infections\n\nTable 9.11: Antiviral drugs"