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Medical Science
Grade 11-12
Antiviral Drugs Reference Cheat Sheet
A printable reference covering viral life cycle targets, antiviral drug classes, mechanisms of action, resistance, and safety basics for grades 11-12.
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Antiviral drugs are medicines that slow or stop viruses from multiplying inside the body. This reference helps students connect each drug class to a specific step in the viral life cycle, such as entry, genome copying, protein processing, or release. It is useful for comparing major antiviral examples and understanding why these medicines must often be used early or in combinations. Students should use it as a study guide for mechanisms, vocabulary, and safe clinical reasoning.
Key Facts
- Antivirals target specific steps in viral replication, including attachment, entry, uncoating, nucleic acid synthesis, protein processing, assembly, and release.
- Nucleoside and nucleotide analogs mimic normal DNA or RNA building blocks and can stop viral genome copying by causing chain termination.
- Acyclovir is activated more efficiently in herpesvirus-infected cells because viral thymidine kinase helps convert it into its active form.
- Neuraminidase inhibitors such as oseltamivir block influenza virus release by inhibiting the viral neuraminidase enzyme.
- Protease inhibitors block viral protein cleavage, so newly made viral particles may remain immature and less infectious.
- Combination antiviral therapy lowers resistance risk because the virus must acquire multiple useful mutations at the same time.
- Antiviral resistance can develop when mutations change the drug target, reduce drug activation, or increase drug removal from infected cells.
- Antibiotics do not treat viral infections because viruses do not have bacterial targets such as cell walls, bacterial ribosomes, or bacterial metabolic pathways.
Vocabulary
- Antiviral drug
- A medicine that reduces viral replication by targeting a virus-specific process or a host process needed by the virus.
- Viral life cycle
- The ordered series of steps a virus uses to enter a cell, copy its genome, make proteins, assemble particles, and spread.
- Nucleoside analog
- A drug that resembles a nucleic acid building block and can interfere with viral DNA or RNA synthesis.
- Protease inhibitor
- A drug that blocks a viral protease enzyme needed to cut viral polyproteins into functional proteins.
- Resistance
- The ability of a virus to keep replicating despite a drug, often because mutations reduce the drug's effectiveness.
- Therapeutic window
- The dose range in which a drug is effective against disease without causing unacceptable toxicity.
Common Mistakes to Avoid
- Thinking antivirals kill viruses directly is wrong because most antivirals mainly slow replication, allowing the immune system to clear infected cells.
- Using antibiotics for a viral infection is wrong because antibiotics target bacterial structures or pathways that viruses do not have.
- Assuming all antivirals work at the same life cycle step is wrong because different drug classes block entry, polymerases, proteases, integrase, or release.
- Stopping antiviral treatment early is risky because remaining viruses may continue replicating and resistant variants may become more common.
- Ignoring timing of treatment is a mistake because many antivirals work best when started early, before viral replication reaches a high level.
Practice Questions
- 1 A virus must use a viral RNA polymerase to copy its genome. Which antiviral drug target would most directly reduce new genome production?
- 2 A patient takes oseltamivir 24 hours after influenza symptoms begin. If the drug reduces release of new virus particles by 70%, what percent of release activity remains?
- 3 A viral population contains 1 resistant virus in every 10,000 viruses. In a sample of 500,000 viruses, how many resistant viruses would be expected?
- 4 Why can combination antiviral therapy reduce the chance of resistance compared with using one antiviral drug alone?