Antiviral drugs – classification and mechanism MCQs With Answer

Antiviral drugs – classification and mechanism MCQs With Answer

Understanding antiviral drugs is essential for B. Pharm students preparing for clinical and pharmaceutical roles. This concise, keyword-rich introduction covers antiviral agents, mechanisms of action, drug classes (entry inhibitors, uncoating inhibitors, nucleoside and nucleotide analogs, polymerase/protease inhibitors, neuraminidase inhibitors, integrase and fusion inhibitors), prodrugs, resistance mechanisms, pharmacokinetics, and safety profiles. Emphasis on molecular targets—reverse transcriptase, viral polymerases, proteases, neuraminidase, and host receptors—helps link theory to therapeutics. These topics are crucial for rational prescribing, drug development, and understanding adverse effects and drug interactions. Now let’s test your knowledge with 30 MCQs on this topic.

Q1. Which of the following best represents a functional classification of antiviral drugs based on molecular mechanism?

• Entry inhibitors, uncoating inhibitors, nucleic acid synthesis inhibitors, and maturation inhibitors
• Analgesics, antipyretics, antiemetics, and antihistamines
• Enzyme activators, receptor agonists, hormone analogs, and vaccines
• Beta-blockers, ACE inhibitors, calcium channel blockers, and diuretics

Correct Answer: Entry inhibitors, uncoating inhibitors, nucleic acid synthesis inhibitors, and maturation inhibitors

Q2. Nucleoside analog antivirals require intracellular phosphorylation to active triphosphate forms; their primary antiviral action is:

• Non-competitive inhibition of host ribosomes
• Chain termination by incorporation into viral DNA/RNA causing premature termination
• Blocking viral entry by binding to cell surface receptors
• Activation of complement leading to viral lysis

Correct Answer: Chain termination by incorporation into viral DNA/RNA causing premature termination

Q3. The main mechanistic difference between NRTIs and NNRTIs used in HIV therapy is:

• NRTIs require phosphorylation and act as chain terminators; NNRTIs bind reverse transcriptase at an allosteric site without phosphorylation
• NNRTIs require phosphorylation and incorporate into viral DNA; NRTIs bind allosterically
• Both classes are protease inhibitors with identical mechanisms
• NRTIs inhibit integrase and NNRTIs inhibit fusion

Correct Answer: NRTIs require phosphorylation and act as chain terminators; NNRTIs bind reverse transcriptase at an allosteric site without phosphorylation

Q4. Which drug is a thymidine analogue NRTI that requires intracellular phosphorylation and is widely used in HIV therapy and prevention of vertical transmission?

• Efavirenz
• Zidovudine
• Ritonavir
• Maraviroc

Correct Answer: Zidovudine

Q5. Protease inhibitors in HIV treatment work by:

• Inhibiting viral neuraminidase to block release of virions
• Blocking cleavage of gag-pol polyproteins, preventing maturation of infectious virions
• Preventing entry by antagonizing host CCR5 receptors
• Inhibiting host cell DNA replication selectively

Correct Answer: Blocking cleavage of gag-pol polyproteins, preventing maturation of infectious virions

Q6. Neuraminidase inhibitors such as oseltamivir limit influenza spread by:

• Inhibiting viral RNA-dependent RNA polymerase directly
• Preventing release of progeny virions from infected cells by blocking viral neuraminidase
• Binding viral M2 ion channel to block uncoating
• Stimulating host interferon production non-specifically

Correct Answer: Preventing release of progeny virions from infected cells by blocking viral neuraminidase

Q7. The antiviral acyclovir is selectively activated in herpes-infected cells because it is initially phosphorylated by:

• Host cell DNA polymerase
• Viral thymidine kinase
• Viral neuraminidase
• Mitochondrial polymerase gamma

Correct Answer: Viral thymidine kinase

Q8. Ganciclovir is preferred over acyclovir for CMV infections primarily because:

• It is activated by bacterial kinases
• It is phosphorylated more efficiently by CMV UL97 kinase and has greater activity against CMV DNA polymerase
• It inhibits neuraminidase rather than polymerase
• It is an oral prodrug with superior bioavailability in CMV

Correct Answer: It is phosphorylated more efficiently by CMV UL97 kinase and has greater activity against CMV DNA polymerase

Q9. Foscarnet is unique among DNA antivirals because it:

• Requires viral kinase activation to be effective
• Acts as a pyrophosphate analog that directly inhibits viral DNA polymerase without phosphorylation
• Is an NNRTI used for HIV treatment
• Enhances viral reverse transcription

Correct Answer: Acts as a pyrophosphate analog that directly inhibits viral DNA polymerase without phosphorylation

Q10. Raltegravir’s primary antiviral mechanism in HIV infection is:

• Inhibition of viral protease
• Inhibition of HIV integrase, preventing proviral DNA integration into host genome
• Blocking CCR5 receptor on host cells
• Inhibiting viral neuraminidase

Correct Answer: Inhibition of HIV integrase, preventing proviral DNA integration into host genome

Q11. Enfuvirtide, a fusion inhibitor, prevents HIV entry by:

• Binding gp41 and inhibiting the conformational changes required for membrane fusion
• Blocking reverse transcriptase polymerase active site
• Inhibiting integrase-mediated integration
• Cleaving viral envelope glycoproteins

Correct Answer: Binding gp41 and inhibiting the conformational changes required for membrane fusion

Q12. Maraviroc exerts its antiviral effect by:

• Binding the CCR5 co-receptor on host cells and blocking R5-tropic HIV entry
• Inhibiting viral protease maturation
• Blocking M2 ion channel of influenza A
• Acting as a nucleoside analog chain terminator

Correct Answer: Binding the CCR5 co-receptor on host cells and blocking R5-tropic HIV entry

Q13. Direct-acting antivirals for hepatitis C commonly target which viral proteins?

• NS3/4A protease, NS5A replication complex, and NS5B RNA-dependent RNA polymerase
• HIV reverse transcriptase and integrase
• Influenza neuraminidase and M2 channel
• Herpes thymidine kinase and UL97 kinase

Correct Answer: NS3/4A protease, NS5A replication complex, and NS5B RNA-dependent RNA polymerase

Q14. Sofosbuvir is best described as:

• An HCV NS5B nucleotide analog inhibitor that is a prodrug converted intracellularly to active triphosphate
• A protease inhibitor that targets HIV Gag-Pol
• A neuraminidase inhibitor used for influenza
• An M2 channel blocker used against influenza B

Correct Answer: An HCV NS5B nucleotide analog inhibitor that is a prodrug converted intracellularly to active triphosphate

Q15. The most common mechanism of viral resistance to acyclovir in herpesviruses involves:

• Upregulation of host thymidine kinase
• Mutations in viral thymidine kinase reducing phosphorylation or mutations in viral DNA polymerase
• Increased neuraminidase expression
• Enhanced drug efflux by viral pumps

Correct Answer: Mutations in viral thymidine kinase reducing phosphorylation or mutations in viral DNA polymerase

Q16. Oseltamivir is administered as a prodrug and is activated primarily by:

• Viral neuraminidase-mediated cleavage
• Host hepatic esterases converting it to the active carboxylate form
• Phosphorylation by viral kinases
• Renal tubular secretion

Correct Answer: Host hepatic esterases converting it to the active carboxylate form

Q17. Which class of antiviral drugs is most associated with mitochondrial toxicity due to inhibition of DNA polymerase gamma?

• NNRTIs
• NRTIs (nucleoside reverse transcriptase inhibitors)
• Protease inhibitors
• Neuraminidase inhibitors

Correct Answer: NRTIs (nucleoside reverse transcriptase inhibitors)

Q18. Ritonavir is frequently used as a pharmacokinetic booster because it:

• Directly kills HIV-infected cells
• Potently inhibits CYP3A4, increasing plasma levels of coadministered protease inhibitors
• Enhances renal excretion of antivirals
• Blocks viral entry via CCR5

Correct Answer: Potently inhibits CYP3A4, increasing plasma levels of coadministered protease inhibitors

Q19. Ribavirin’s antiviral effects include inhibition of IMP dehydrogenase leading to decreased GTP pools and:

• Direct inhibition of viral protease maturation
• Lethal mutagenesis of RNA viruses and broad-spectrum activity including RSV and HCV
• Activation of viral neuraminidase
• Specific inhibition of HIV integrase

Correct Answer: Lethal mutagenesis of RNA viruses and broad-spectrum activity including RSV and HCV

Q20. Amantadine’s antiviral action against influenza A is mediated through:

• Inhibition of neuraminidase activity
• Blockade of the M2 proton channel, preventing viral uncoating
• Activation of host interferon pathways
• Inhibition of viral reverse transcriptase

Correct Answer: Blockade of the M2 proton channel, preventing viral uncoating

Q21. Cidofovir differs from many nucleoside antivirals because it:

• Is a nucleotide analog that does not require initial phosphorylation by viral kinases and inhibits viral DNA polymerase
• Is an NNRTI that requires no phosphorylation and targets integrase
• Is a neuraminidase inhibitor with oral prodrug formulation
• Acts as a host CCR5 antagonist

Correct Answer: Is a nucleotide analog that does not require initial phosphorylation by viral kinases and inhibits viral DNA polymerase

Q22. Resistance to neuraminidase inhibitors typically arises from:

• Mutations in viral neuraminidase that reduce drug binding while retaining enzymatic function
• Overexpression of host esterases that activate the prodrug too rapidly
• Loss of viral envelope entirely
• Acquisition of bacterial co-infection genes

Correct Answer: Mutations in viral neuraminidase that reduce drug binding while retaining enzymatic function

Q23. Valacyclovir has improved oral bioavailability compared to acyclovir because it is:

• A neuraminidase inhibitor rather than a nucleoside analog
• An L-valyl ester prodrug of acyclovir that undergoes rapid first-pass hydrolysis to acyclovir
• Less polar and acts as a protease inhibitor
• Activated by bacterial enzymes in the gut

Correct Answer: An L-valyl ester prodrug of acyclovir that undergoes rapid first-pass hydrolysis to acyclovir

Q24. Interferons exert antiviral activity mainly by:

• Directly inhibiting viral proteases
• Inducing host antiviral proteins, enhancing MHC expression, and activating innate immune responses
• Blocking viral neuraminidase
• Converting nucleoside analogs to their active forms

Correct Answer: Inducing host antiviral proteins, enhancing MHC expression, and activating innate immune responses

Q25. Baloxavir marboxil, a newer influenza antiviral, inhibits:

• Neuraminidase cleavage of sialic acid
• The cap-dependent endonuclease of viral polymerase, blocking viral mRNA synthesis
• M2 proton channel activity
• Reverse transcriptase

Correct Answer: The cap-dependent endonuclease of viral polymerase, blocking viral mRNA synthesis

Q26. A clinically significant adverse effect of ribavirin therapy is:

• Cardiac arrhythmias as the primary toxicity
• Hemolytic anemia due to accumulation of ribavirin in erythrocytes
• Severe neurotoxicity causing seizures in all patients
• Marked nephrotoxicity requiring dialysis in most cases

Correct Answer: Hemolytic anemia due to accumulation of ribavirin in erythrocytes

Q27. HCV NS3/4A protease inhibitors (e.g., simeprevir) principally act by:

• Inhibiting viral entry via CCR5 blockade
• Preventing polyprotein processing necessary for viral replication complex formation
• Inhibiting host DNA polymerase gamma selectively
• Acting as neuraminidase inhibitors

Correct Answer: Preventing polyprotein processing necessary for viral replication complex formation

Q28. Tenofovir disoproxil fumarate is classified as:

• An NNRTI
• A nucleotide reverse transcriptase inhibitor (NtRTI) that is a prodrug of tenofovir
• A protease inhibitor used for influenza
• An M2 channel blocker specific for influenza B

Correct Answer: A nucleotide reverse transcriptase inhibitor (NtRTI) that is a prodrug of tenofovir

Q29. The rationale for designing antiviral prodrugs (e.g., valacyclovir, oseltamivir) is primarily to:

• Increase drug polarity and decrease absorption
• Enhance oral bioavailability, tissue penetration, or selective activation in target cells
• Prevent metabolism entirely so drugs remain unchanged
• Make drugs resistant to all viral mutations

Correct Answer: Enhance oral bioavailability, tissue penetration, or selective activation in target cells

Q30. For optimal effectiveness, oseltamivir should ideally be initiated within what time frame after influenza symptom onset?

• Within 48 hours
• After 7 days
• Only after negative rapid antigen test
• At least 5 days post-symptom onset for maximal effect

Correct Answer: Within 48 hours

G S Sachin

I am a Registered Pharmacist under the Pharmacy Act, 1948, and the founder of PharmacyFreak.com. I hold a Bachelor of Pharmacy degree from Rungta College of Pharmaceutical Science and Research. With a strong academic foundation and practical knowledge, I am committed to providing accurate, easy-to-understand content to support pharmacy students and professionals. My aim is to make complex pharmaceutical concepts accessible and useful for real-world application.

Mail- Sachin@pharmacyfreak.com