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Quizzes > Health & Medicine > Human Anatomy & Medicine

Antiviral Drugs Trivia: Can You Spot the True Statement?

Think You Know Drug Specificity? Which Antiviral Drugs May Target All of the Following Except

Difficulty: Moderate
2-5mins
Learning OutcomesCheat Sheet
Paper art illustration of capsules and virus shapes on dark blue background for antiviral drugs quiz

This quiz helps you confirm which statements about antiviral medications are true. Work through quick items on drug targets, viral replication steps, and common side effects to sharpen recall. When you finish, keep learning with more pharmacology practice or try more true-or-false questions.

What is the primary mechanism of action of most antiviral medications?
They kill host cells to stop infection
They inhibit viral replication enzymes
They neutralize bacterial toxins
They disrupt bacterial cell walls
Antiviral drugs primarily target viral enzymes to prevent the virus from replicating in host cells. Most antivirals inhibit viral polymerases or proteases essential for genome replication. This specific targeting reduces harm to host cells.
Which type of pathogen are antiviral drugs designed to treat?
Fungi
Viruses
Bacteria
Parasites
Antiviral medications are specifically formulated to target viruses and their replication processes. They have no effect on bacterial, fungal, or parasitic organisms. This specificity is why antibiotics are ineffective against viral infections.
Which drug class is commonly used to treat influenza A and B?
Azoles
Macrolides
Penicillins
Neuraminidase inhibitors
Neuraminidase inhibitors, such as oseltamivir and zanamivir, block the viral neuraminidase enzyme, preventing influenza virus release from infected cells. They are effective against both influenza A and B.
Which antiviral is most commonly prescribed for herpes simplex virus infections?
Acyclovir
Ivermectin
Fluconazole
Amoxicillin
Acyclovir is a nucleoside analog that inhibits viral DNA polymerase, making it first-line therapy for herpes simplex virus types 1 and 2. It reduces viral replication and symptom duration.
Which statement about antiviral medications versus antibiotics is true?
Both kill viruses directly
Antivirals target viral processes, antibiotics target bacterial processes
Antibiotics are effective against viruses
Antivirals strengthen bacterial cell walls
Antivirals are designed to interfere with viral replication or entry, whereas antibiotics act on bacterial cell walls, ribosomes, or other bacterial-specific targets. Antibiotics have no effect on viruses.
Which route of administration is most common for systemic antiviral drugs?
Transdermal patch
Topical
Oral
Inhalation
Most systemic antiviral medications are formulated for oral administration to ensure adequate absorption and patient compliance. Some specialized antivirals may use other routes.
Which of the following is a broad-spectrum antiviral?
Ketoconazole
Penicillin
Ribavirin
Isoniazid
Ribavirin exhibits activity against a wide range of RNA viruses including RSV, hepatitis C, and some hemorrhagic fever viruses, making it a broad-spectrum antiviral.
Which cellular component do most nucleoside analog antivirals mimic?
Fatty acids
Amino acids
Nucleotides
Carbohydrates
Nucleoside analogs resemble natural nucleotides and get incorporated into viral nucleic acids, causing chain termination or mutation and halting viral replication.
Which antiviral class is primarily used in HIV therapy to prevent viral protease activity?
Fusion inhibitors
Protease inhibitors
Integrase inhibitors
Neuraminidase inhibitors
Protease inhibitors block the HIV protease enzyme, preventing cleavage of viral polyproteins and production of mature virions, a cornerstone of antiretroviral therapy.
Which antiviral drug requires phosphorylation by viral thymidine kinase for activation?
Ritonavir
Zidovudine
Acyclovir
Oseltamivir
Acyclovir is initially phosphorylated by viral thymidine kinase, then by cellular kinases to its active triphosphate form, which inhibits viral DNA polymerase.
Which virus is treated with the drug sofosbuvir?
Hepatitis C virus
Herpes simplex virus
Human papillomavirus
Influenza A virus
Sofosbuvir is a nucleotide analog inhibitor of the HCV RNA polymerase NS5B, used in combination regimens to cure chronic hepatitis C infection.
Which statement about antiviral resistance is true?
Resistance is irreversible in all viruses
Host cells develop resistance
Resistance can arise from viral enzyme mutations
Resistance only occurs in bacteria
Viruses can mutate the genes encoding target enzymes like polymerases or proteases, reducing drug binding and leading to antiviral resistance. Monitoring and rotating drugs can help manage resistance.
Which direct-acting antiviral class inhibits the NS5A protein of hepatitis C virus?
Nucleos(t)ide polymerase inhibitors
Entry inhibitors
NS5A inhibitors
NS3/4A protease inhibitors
NS5A inhibitors block a nonstructural protein critical for hepatitis C virus replication and assembly. Drugs like ledipasvir belong to this class, enhancing cure rates when combined.
Which antiviral drug is a fusion inhibitor used against HIV entry?
Ritonavir
Lamivudine
Enfuvirtide
Amantadine
Enfuvirtide binds to the gp41 subunit of HIV-1, preventing fusion of the viral and host cell membranes. It is used in treatment-experienced patients with resistant HIV.
Which antiviral class blocks the M2 ion channel of influenza A virus?
Protease inhibitors
Neuraminidase inhibitors
Adamantanes
Integrase inhibitors
Adamantanes such as amantadine and rimantadine inhibit the M2 proton channel of influenza A, blocking viral uncoating. Their use is limited by widespread resistance.
Which drug combination is a common fixed-dose regimen for HIV pre-exposure prophylaxis?
Tenofovir disoproxil fumarate/emtricitabine
Efavirenz/tenofovir
Darunavir/ritonavir
Zidovudine/lamivudine
The tenofovir disoproxil fumarate/emtricitabine fixed-dose combination is approved for PrEP, reducing HIV acquisition risk in high-risk individuals.
Which enzyme do HIV integrase inhibitors block?
Viral integrase
Neuraminidase
Reverse transcriptase
Protease
Integrase inhibitors such as raltegravir prevent incorporation of viral DNA into the host genome by blocking the HIV integrase enzyme, a critical step in viral replication.
Which drug is a non-nucleoside reverse transcriptase inhibitor (NNRTI)?
Stavudine
Lamivudine
Zidovudine
Efavirenz
Efavirenz binds directly to reverse transcriptase at a site distinct from the active site, causing conformational changes that inhibit enzyme activity.
Which antiviral requires renal dosing adjustments due to accumulation of its active metabolite?
Acyclovir
Oseltamivir
Zanamivir
Sofosbuvir
Acyclovir and its prodrug valacyclovir are excreted by the kidneys; renal impairment can lead to toxic accumulation, requiring dose adjustment.
Which mechanism best describes how interferon therapy exerts antiviral effects?
Destroys viral RNA directly
Blocks viral integrase
Stimulates host antiviral gene expression
Directly inhibits viral neuraminidase
Interferons bind to host receptors and activate transcription of interferon-stimulated genes, creating an antiviral state in cells that inhibits replication of many viruses.
Which antiviral agent is an entry inhibitor that binds to CCR5 co-receptor on host cells?
Maraviroc
Lopinavir
Amantadine
Zidovudine
Maraviroc blocks the CCR5 chemokine receptor on CD4+ cells, preventing R5-tropic HIV strains from attaching and entering host cells.
Which term describes the lowest concentration of drug that inhibits viral replication in vitro?
LD50
CC50
EC50
MIC
EC50 (effective concentration 50%) is the concentration at which a drug achieves half its maximal inhibitory effect on viral replication in cell culture assays.
Which of the following antivirals is an example of a prodrug?
Oseltamivir carboxylate
Ribavirin
Valacyclovir
Zanamivir
Valacyclovir is converted by first-pass metabolism to acyclovir, increasing oral bioavailability compared to the parent compound.
Which antiviral agent is specifically indicated for respiratory syncytial virus (RSV) in high-risk infants?
Palivizumab
Acyclovir
Oseltamivir
Ribavirin
Palivizumab is a monoclonal antibody given prophylactically to high-risk infants to prevent severe RSV disease by neutralizing the virus before cell entry.
Which mutation in HIV reverse transcriptase confers high-level resistance to zidovudine?
L90M
M184V
T215Y
K103N
The T215Y mutation in HIV-1 reverse transcriptase reduces incorporation of zidovudine triphosphate, leading to high-level resistance. Monitoring genotypes guides therapy adjustments.
Which pharmacokinetic property is most important for determining dosing intervals of antivirals?
Volume of distribution
Half-life
Bioavailability
Protein binding
The elimination half-life of a drug determines how long effective plasma concentrations are maintained and thus guides dosing frequency to stay within the therapeutic window.
Which molecular change in influenza virus can lead to reduced efficacy of neuraminidase inhibitors?
K65R in PB2 gene
M2 S31N mutation
D614G in HA gene
H275Y in NA gene
The H275Y substitution in the neuraminidase gene alters the active site, reducing binding of oseltamivir and conferring resistance.
Which drug interaction can increase plasma concentrations of protease inhibitors via CYP3A4 inhibition?
Ritonavir with phenytoin
Ritonavir with ketoconazole
Ritonavir with rifampin
Ritonavir with carbamazepine
Ketoconazole is a potent CYP3A4 inhibitor, and when co-administered with ritonavir, it can raise ritonavir levels, increasing toxicity risk. Conversely, inducers like rifampin lower levels.
Which advanced assay measures viral load for monitoring hepatitis C therapy?
Hemagglutination inhibition
ELISA
Quantitative PCR
Western blot
Quantitative real-time PCR accurately measures HCV RNA copies per mL, allowing assessment of viral kinetics and treatment response.
Which characteristic defines a high genetic barrier to resistance in antiviral therapy?
Drug eliminated rapidly
Low protein binding
Multiple mutations required
Single point mutation confers resistance
High genetic barrier means the virus must accumulate several mutations before significant resistance emerges, reducing the chance of treatment failure.
Which antiviral drug is activated by host alkaline phosphatases rather than kinases?
Adefovir dipivoxil
Zidovudine
Tenofovir alafenamide
Abacavir
Tenofovir alafenamide is hydrolyzed by host cathepsin A and carboxylesterase in lymphoid cells, not requiring phosphorylation by kinases, leading to targeted activation.
Which technique assesses the binding affinity of an antiviral to its viral target in drug development?
Hemagglutination assay
Western blot
Surface plasmon resonance
ELISA
Surface plasmon resonance measures real-time interactions between molecules, providing kinetic data on association and dissociation rates of antiviral compounds and their targets.
Which property of remdesivir allows it to evade viral exonuclease proofreading in coronaviruses?
C-nucleoside structure
Blocking fusion
Inhibition of neuraminidase
Binding to protease
Remdesivir's adenosine analog has a C-nucleoside structure that is poorly recognized by the viral exonuclease, allowing it to incorporate into RNA and cause delayed chain termination.
Which molecular feature increases the oral bioavailability of a prodrug?
High ionization
Large molecular weight
Increased lipophilicity
Low plasma protein binding
Enhancing lipophilicity promotes passive diffusion across gastrointestinal membranes, improving absorption and oral bioavailability of prodrugs.
Which drug development phase primarily assesses antiviral safety in healthy volunteers?
Phase I
Phase IV
Phase II
Phase III
Phase I trials focus on safety, tolerability, pharmacokinetics, and dosing in a small group of healthy volunteers before efficacy studies.
Which host factor is targeted by cyclophilin inhibitors to block hepatitis C replication?
Integrin ?4?7
CD4 receptor
CCR5 co-receptor
Cyclophilin A
Cyclophilin A is a host peptidyl-prolyl isomerase that assists HCV replication; inhibitors disrupt its interaction with viral proteins, reducing replication.
Which strategy uses CRISPR/Cas systems to target and degrade viral genomes in infected cells?
Monoclonal antibody therapy
Gene editing antiviral therapy
Protease inhibitor therapy
RNA interference
CRISPR/Cas-based therapies are engineered to recognize viral DNA or RNA sequences and induce targeted cleavage, offering a novel approach to clear persistent infections.
Which computational method predicts antiviral drug binding to novel viral proteins by simulating molecular interactions?
ELISPOT assay
Molecular docking
Western blot
Flow cytometry
Molecular docking uses algorithms to predict the optimal orientation and binding energy of small molecules with target proteins, accelerating antiviral drug discovery.
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Study Outcomes

  1. Understand Antiviral Drug Mechanisms -

    Explain how different classes of antiviral medications interfere with viral replication processes, from entry inhibitors to polymerase blockers.

  2. Identify True Statements About Antiviral Medications -

    Distinguish accurate facts from misconceptions by evaluating key features of antiviral therapies.

  3. Differentiate Drug Specificity and Spectrum of Activity -

    Compare broad-spectrum versus narrow-spectrum antivirals and their targeted viral families.

  4. Analyze Common Side Effects and Toxicity Profiles -

    Assess safety considerations by reviewing typical adverse reactions associated with major antiviral drugs.

  5. Apply Knowledge to "Except" Questions -

    Determine which viral targets or processes are not affected by specific antiviral agents in quiz scenarios.

  6. Evaluate Quiz Results for Self-Assessment -

    Use your quiz performance to identify knowledge gaps and reinforce understanding of antiviral drug principles.

Cheat Sheet

  1. Mechanism: Viral Polymerase Inhibitors -

    Antivirals like acyclovir and sofosbuvir are activated to nucleotide analogs that interrupt viral DNA or RNA polymerization, ensuring selective toxicity (CDC, 2021). Acyclovir requires viral thymidine kinase, exemplifying virus-specific activation. Memory trick: "Ava the Analog halts the viral Pol."

  2. Target Specificity and Narrow Spectrum -

    Most antivirals have a narrow spectrum, targeting unique viral proteins such as HIV protease or influenza neuraminidase (WHO, 2022). While antiviral drugs may target all of the following except peptidoglycan cell walls, they specifically inhibit processes like viral assembly. Knowing this helps nail questions like "which statement regarding antiviral medications is true" on your next antiviral drugs quiz.

  3. Resistance through Viral Mutations -

    Resistance often arises from point mutations in viral enzymes that reduce drug binding, such as the K103N mutation in HIV reverse transcriptase (NEJM, 2019). Regular genotypic testing guides regimen changes to overcome resistance. Mnemonic: "Key 103 locks out the inhibitor."

  4. Side Effects and Selective Toxicity -

    Side effects vary widely; for instance, ganciclovir can cause bone marrow suppression while oseltamivir may lead to mild gastrointestinal upset (AMA Journal, 2020). Understanding selective toxicity principles allows you to predict adverse events based on drug target and host cell overlap. This insight is crucial for the antiviral medication side effects quiz section.

  5. Broad-Spectrum Agents and Host Modulators -

    Although most antivirals are virus-specific, some host-targeting broad-spectrum agents like interferons or ribavirin can impact multiple viruses by boosting innate immunity or inhibiting RNA capping (NIH, 2021). This dual approach underscores why broad-spectrum options remain limited compared to narrow-spectrum inhibitors. Perfect prep for your antiviral drug mechanisms quiz, as you'll answer why true antiviral breadth is rare.

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