Antiviral drugs are designed to target specific stages of the viral replication cycle, disrupting the virus’s ability to infect and replicate within host cells. The viral replication cycle typically involves several key steps, and antiviral drugs are developed to interfere with these processes.

  1. Attachment and Entry:
    • Target: Viral attachment proteins or host cell receptors.
    • Antiviral Action: Some drugs prevent viruses from attaching to host cells by targeting viral surface proteins or host cell receptors. These drugs may block the interaction between the virus and the host cell, preventing viral entry. Example: Oseltamivir (Tamiflu) inhibits the neuraminidase enzyme of influenza viruses, preventing their attachment to host cells and subsequent entry.
  2. Fusion:
    • Target: Viral fusion proteins.
    • Antiviral Action: Fusion inhibitors interfere with the fusion of viral and cellular membranes, preventing the virus from entering the host cell. These drugs are particularly effective against enveloped viruses. Example: Enfuvirtide (Fuzeon) is a fusion inhibitor used against HIV, blocking the fusion of viral and cellular membranes.
  3. Reverse Transcription (for retroviruses):
    • Target: Reverse transcriptase enzyme.
    • Antiviral Action: Retroviruses, such as HIV, use reverse transcriptase to convert their RNA genome into DNA. Reverse transcriptase inhibitors block this process, preventing the formation of viral DNA and subsequent integration into the host cell genome. Example: Zidovudine (AZT) is a nucleoside reverse transcriptase inhibitor (NRTI) that interferes with the reverse transcription step in the replication of HIV.
  4. Transcription and Translation:
    • Target: Viral RNA or DNA polymerase, and viral proteins.
    • Antiviral Action: Nucleoside and nucleotide analogs interfere with the synthesis of viral nucleic acids by mimicking building blocks. Non-nucleoside analogs may target viral polymerase enzymes directly. Inhibiting transcription and translation disrupts the production of viral genetic material and proteins. Example: Remdesivir is a broad-spectrum antiviral that acts as an RNA polymerase inhibitor, disrupting viral RNA synthesis. It has been used against various RNA viruses, including SARS-CoV-2.
  5. Maturation and Assembly:
    • Target: Viral protease.
    • Antiviral Action: Protease inhibitors block the activity of viral protease enzymes, preventing the cleavage of viral polyproteins into functional components. This disruption inhibits the formation of mature and infectious viral particles. Example: Protease inhibitors like Lopinavir inhibit the viral protease enzyme, preventing the cleavage of viral polyproteins during the maturation of viruses like HIV
  6. Release:
    • Target: Viral release mechanisms.
    • Antiviral Action: Some drugs interfere with the release of new virions from infected cells. For example, neuraminidase inhibitors prevent the release of influenza virus from host cells by inhibiting the neuraminidase enzyme. Example: Oseltamivir (Tamiflu) and Zanamivir (Relenza) inhibit the neuraminidase enzyme, disrupting the release of new influenza virus particles from infected cells.

It’s important to note that not all antiviral drugs target all stages of the viral replication cycle. Additionally, the development of antiviral drugs is often specific to particular viruses, and a drug effective against one virus may not be effective against others. Combination therapies targeting multiple stages of the viral life cycle are sometimes used to increase efficacy and reduce the risk of drug resistance.

Further Reading,

  1. A review: Mechanism of action of antiviral drugs
  2. Mechanism of Action of Antiviral Drugs
  3. Antiviral Classification
  4. HIV Antiretroviral Therapy
  5. Antiviral Agents