15.1 Classes of antiviral drugs and their mechanisms of action
5 min read•august 1, 2024
Antiviral drugs are crucial weapons against viral infections. They target different stages of the viral life cycle, from entry to replication and release. Understanding their mechanisms helps us develop better treatments and combat drug resistance.
Classes of antivirals include nucleic acid synthesis inhibitors, protein processing blockers, and . Each class works differently, like stopping viral DNA replication or preventing virus release. Knowing these differences is key to effective treatment strategies.
Antiviral Drug Classes and Targets
Nucleic Acid Synthesis Inhibitors
Top images from around the web for Nucleic Acid Synthesis Inhibitors
Mechanisms of Other Antimicrobial Drugs | Microbiology View original
Is this image relevant?
Frontiers | Transcription and Translation Inhibitors in Cancer Treatment View original
Is this image relevant?
Frontiers | The Signaling Pathways, and Therapeutic Targets of Antiviral Agents: Focusing on the ... View original
Is this image relevant?
Mechanisms of Other Antimicrobial Drugs | Microbiology View original
Is this image relevant?
Frontiers | Transcription and Translation Inhibitors in Cancer Treatment View original
Is this image relevant?
1 of 3
Top images from around the web for Nucleic Acid Synthesis Inhibitors
Mechanisms of Other Antimicrobial Drugs | Microbiology View original
Is this image relevant?
Frontiers | Transcription and Translation Inhibitors in Cancer Treatment View original
Is this image relevant?
Frontiers | The Signaling Pathways, and Therapeutic Targets of Antiviral Agents: Focusing on the ... View original
Is this image relevant?
Mechanisms of Other Antimicrobial Drugs | Microbiology View original
Is this image relevant?
Frontiers | Transcription and Translation Inhibitors in Cancer Treatment View original
Is this image relevant?
1 of 3
target viral DNA or RNA polymerases inhibiting viral genome replication
Incorporate into growing viral nucleic acid chain causing chain termination or mutations
Examples include (herpes viruses) and (respiratory syncytial virus, hepatitis C)
directly interfere with viral RNA or DNA polymerases preventing viral genome replication
Act as nucleoside analogs or allosteric inhibitors disrupting polymerase function
Examples include (hepatitis C) and ()
Protein Processing and Function Inhibitors
interfere with viral protease enzymes preventing the cleavage of viral polyproteins into functional proteins
Bind to active site of viral proteases blocking polyprotein processing
Examples include () and (hepatitis C)
target the neuraminidase enzyme of influenza viruses inhibiting viral release from infected cells
Mimic sialic acid blocking enzyme activity and preventing virion release
Examples include and (influenza A and B)
Retrovirus-Specific Inhibitors
specifically target the reverse transcriptase enzyme of retroviruses blocking the conversion of viral RNA to DNA
Nucleoside or non-nucleoside based incorporating into DNA chain or allosterically inhibiting enzyme
Examples include (AZT) and (HIV)
block the integration of viral DNA into the host cell genome primarily used against retroviruses like HIV
Bind to active site of integrase enzyme preventing viral DNA insertion
Examples include raltegravir and dolutegravir (HIV)
Entry and Fusion Inhibitors
Entry inhibitors prevent viral attachment fusion or entry into host cells by targeting viral envelope proteins or host cell receptors
Block receptor binding prevent membrane fusion or inhibit conformational changes for
Examples include (HIV) and (HIV CCR5 antagonist)
Mechanisms of Antiviral Action
Competitive Inhibition and Substrate Mimicry
Nucleoside/nucleotide analogs act as competitive inhibitors incorporating into growing viral nucleic acid chain
Cause chain termination or induce mutations in viral genome
Structurally similar to natural nucleosides but lack 3' hydroxyl group for chain extension
Neuraminidase inhibitors mimic sialic acid the natural substrate of neuraminidase blocking enzyme's activity
Prevent release of newly formed virus particles from infected cells
Bind to active site with higher affinity than natural substrate
Enzyme Active Site Binding
Protease inhibitors bind to active site of viral proteases preventing cleavage of viral polyproteins
Block formation of functional structural and enzymatic components
Often designed to mimic transition state of protease-substrate complex
Integrase inhibitors bind to active site of integrase enzyme preventing insertion of viral DNA into host genome
Interfere with strand transfer step of integration process
Stabilize integrase-viral DNA complex preventing interaction with host DNA
Allosteric Inhibition
Non-nucleoside reverse transcriptase inhibitors allosterically inhibit enzyme function
Bind to site distant from active site inducing conformational changes
Reduce enzyme flexibility and catalytic activity
Some polymerase inhibitors act as allosteric inhibitors altering enzyme conformation
Bind to sites outside the catalytic center affecting polymerase function
May interfere with protein-protein interactions or substrate binding
Antiviral Interference with Replication
Targeting Specific Replication Stages
Entry inhibitors prevent initial steps of infection blocking viral attachment fusion or entry
Halt replication cycle before it begins in host cell
Examples include (enfuvirtide) and receptor antagonists (maraviroc)
Reverse transcriptase and integrase inhibitors interfere with early post-entry steps in retrovirus replication
Prevent establishment of proviral DNA in host genome
Critical for blocking retroviral life cycle (HIV)
Disrupting Genome Replication and Protein Processing
Nucleoside/nucleotide analogs and polymerase inhibitors disrupt genome replication
Interfere with synthesis of new viral DNA or RNA
Can induce lethal mutagenesis or premature chain termination
Protease inhibitors act during late stages of viral replication cycle
Prevent maturation of viral proteins necessary for assembly of infectious particles
Result in production of non-infectious viral particles
Blocking Virus Release and Spread
Neuraminidase inhibitors interfere with final stage of influenza virus replication
Prevent release of newly formed virions from infected cells
Reduce viral spread to neighboring cells
Targeting different stages of viral replication cycle effectively reduces viral load