22 topics with concise breakdowns: definitions, key facts, and classroom questions.
Antiviral drugs are one of the most rapidly developing fields in pharmacology. In this module, we examine the classification, pharmacodynamics, and clinical use of drugs that inhibit viral replication at various stages of their life cycle.
The section covers core groups: antiherpetic agents (from classic acyclovir to cidofovir and foscarnet), an extensive block of antiretroviral therapy for HIV (reverse transcriptase, protease, integrase, and entry inhibitors), anti-influenza drugs, interferons, and hepatitis B therapy and immunoprophylaxis. Historically, malaria pathogens have also found their way into this curriculum module — be prepared for this terminological surprise.
In classes and exams, mechanisms of action are tested most rigorously. Be sure to understand how viral thymidine kinase activates acyclovir, the differences between nucleoside and non-nucleoside reverse transcriptase inhibitors in HIV, and why adamantane derivatives have lost relevance in favor of neuraminidase inhibitors. Pay special attention to side effects — for instance, the myelosuppressive effect of zidovudine and ganciclovir.
How do acyclic nucleosides differ structurally from natural analogues?
They are created on the basis of purine nucleosides (guanine), but instead of a complete closed sugar ring, they have an open acyclic carbohydrate chain.
Why is acyclovir safe for healthy body cells?
Initial phosphorylation of the drug is carried out exclusively by viral thymidine kinase. Uninfected cells lack this enzyme, so the drug remains in the form of an inactive prodrug.
What is the main structural difference between penciclovir and acyclovir?
Its acyclic side chain contains a 3'-hydroxyl group. This very group determines the specific features of the drug's interaction with viral DNA during synthesis.
Why cannot idoxuridine be administered orally or via injection?
The drug exhibits high toxicity, which is why it is used exclusively topically.
Why is ganciclovir prescribed for CMV infection instead of the safer acyclovir?
Cytomegalovirus lacks the thymidine kinase enzyme required to activate acyclovir. Ganciclovir, however, can be activated by a specific viral phosphotransferase (encoded by the UL97 gene), which is why it works against CMV.
What is the main difference in the chemical structure of cidofovir from classic nucleosides?
Cidofovir is a nucleotide analogue and already contains a single phosphate group in its structure, which frees it from the need for initial phosphorylation by viral enzymes.
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