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Anti-viral Agents

Classes of Anti-viral Medications

© Judy Arbique

Dec 25, 2006
Anti-viral agents inhibit viral replication rather than eliminating viral particles already present.

The process of viral replication is specific to the type of virus, but in all cases replication is reliant on unique enzymes that are essential for viral replication and are not involved in normal cellular function. Processes unique to viral replication are the best targets for antiviral agents.

Enzymes that are common to cellular metabolism and viral replication can also be targeted in some cases. For example, thymidine kinase is an enzyme utilized in both cellular metabolism and viral replication, and can be exploited to activate antiviral agents.

Viral attachment, penetration, assembly and release processes are catalyzed by cellular enzymes, making it difficult to selectively inhibit these processes without adversely affecting normal cell metabolism.

There are four classes of anti-viral medications:

  • Non-nucleoside reverse transcriptase inhibitors
  • Nucleoside reverse transcriptase inhibitors (nucleoside analogs)
  • Protease inhibitors
  • Nucleotide analog reverse transcriptase inhibitors (NtARTIs or NtRTIs)

Each class of drug attacks a different phase in the life cycle of the virus.

Non-nucleoside reverse transcriptase inhibitor (NNRTI):

  • Nevirapine [Viramune®]
  • Delavirdine [Rescriptor®]
  • Efavirenz [Sustiva® and Stocrin®]

NNRTIs bind to reverse transcriptase, blocking DNA polymerase required to convert viral RNA to DNA.

Nucleoside reverse transcriptase inhibitor (NRTI):

  • Zidovudine [AZT, ZDV, azidothymidine, Retrovir®]
  • Didanosine [ddI, Videx® Videx EC®]
  • Zalcitabine [ddC, deoxycytidine, Hivid®]
  • Stavudine [d4T, Zerit®, Zerit XR®]
  • Lamivudine [3TC, Epivir®]
  • Abacavir [ABC, Ziagen®]
  • Emtricitabine [FTC, Emtriva®, Coviracil])

NRTIs interrupt the formation of viral DNA from RNA by substituting a look-alike compound (analog) that resembles nucleosides (building blocks) used by the virus to synthesize DNA. DNA cannot be synthesized from the look-alike compound and the virus is blocked from replicating.

Protease inhibitors (PIs):

  • Amprenavir [Agenerase]
  • Fosamprenavir [Lexiva]
  • Indinavir [Crixivan] Iopinavir/ritonavir [Kaletra]
  • Ritonavir [Norvir]
  • Saquinavir [Fortovase]
  • Nelfinavir [Viracept]Protease inhibitors block protease, the enzyme that cuts viral protein into segments and assembles the segments around viral RNA to form infectious viral particles. Inhibition of protease results in non-infectious virus particles.Nucleotide analog reverse transcriptase inhibitors (NtARTIs or NtRTIs)
    • Tenofovir [tenofovir disoproxil fumarate, Viread®]
    • Adefovir [bis-POM PMPA, Preveon® and Hepsera®])
    Whereas nucleoside analogs are converted into nucleotide analogs during cellular metabolism, NtARTIs do not require cellular activation. NtARTIs result in less toxicity than NRTIs.

    • The copyright of the article Anti-viral Agents in Microbiology is owned by Judy Arbique. Permission to republish Anti-viral Agents in print or online must be granted by the author in writing.




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