Entry inhibitors (EIs) |
They interfere with binding, fusion, and entry of HIV-1 to the host cell |
CCR5 receptor antagonists (CCR5RAs) |
They bind to the CCR5 receptor on the surface of the T-Cell and block viral attachment to the cell. If HIV cannot attach to the cell, it cannot gain entry to replicate |
Nucleoside reverse transcriptase inhibitors (NsRTIs) and nucleotide reverse transcriptase inhibitors (NtRTIs) |
They inhibit reverse transcription by being incorporated into the newly synthesized viral DNA strand as faulty nucleotides; they both act as competitive substrate inhibitors |
Non-nucleoside reverse transcriptase inhibitors (NNRTIs) |
They inhibit reverse transcriptase by binding to an allosteric site of the enzyme; NNRTIs act as non-competitive inhibitors of reverse transcriptase |
Protease inhibitors (PIs) |
They target viral assembly by inhibiting the activity of protease, an enzyme used by HIV to cleave nascent proteins for the final assembly of new virions |
Integrase inhibitors (IIs) |
They inhibit the enzyme integrase, which is responsible for integration of viral DNA into the DNA of the infected cell |
Maturation inhibitors (MIs) |
They inhibit the last step in gag processing in which the viral capsid polyprotein is cleaved, thereby blocking the conversion into mature capsid protein |