Infections: bacterial, viral, fungal, parasitic: imiquimod in anogenital warts: practice question

A Dermatology question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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Dermatology · Infections: bacterial, viral, fungal, parasitic: imiquimod in anogenital warts

Sample item

A topical immune response modifier is applied three nights a week for anogenital warts and clears them without being directly cytotoxic. What is its mechanism of action?

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

D. Toll-like receptor 7 agonist inducing local interferon release

Imiquimod stimulates toll-like receptor 7 on dendritic cells and macrophages, inducing interferon-alpha, TNF-alpha and interleukin-12 so that local innate and cell-mediated immunity clears HPV-infected cells. Local inflammation and erythema are common side effects.

Option by option

  • A. Inhibiting viral DNA polymerase as a nucleoside analogue

    Nucleoside analogues such as acyclovir act on herpesvirus polymerase and do not treat HPV warts.

  • B. Binding to tubulin and arresting cell division in metaphase

    Tubulin binding and mitotic arrest describe podophyllotoxin, a directly cytotoxic agent.

  • C. Dissolving intercellular keratin cement as a keratolytic

    Keratolysis describes salicylic acid and does not recruit immunity.

  • D. Toll-like receptor 7 agonist inducing local interferon release (correct)

    Correct. TLR-7 stimulation drives local cytokine release and a cell-mediated antiviral response.

Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.

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Questions about this Dermatology question

What is the answer to this Dermatology question?

The best answer is D, Toll-like receptor 7 agonist inducing local interferon release. Imiquimod stimulates toll-like receptor 7 on dendritic cells and macrophages, inducing interferon-alpha, TNF-alpha and interleukin-12 so that local innate and cell-mediated immunity clears HPV-infected cells.

Why is "Inhibiting viral DNA polymerase as a nucleoside analogue" not the answer?

Nucleoside analogues such as acyclovir act on herpesvirus polymerase and do not treat HPV warts.

Why is "Binding to tubulin and arresting cell division in metaphase" not the answer?

Tubulin binding and mitotic arrest describe podophyllotoxin, a directly cytotoxic agent.

Why is "Dissolving intercellular keratin cement as a keratolytic" not the answer?

Keratolysis describes salicylic acid and does not recruit immunity.

What concept does this question test?

It tests Infections: bacterial, viral, fungal, parasitic: imiquimod in anogenital warts in Dermatology. Local inflammation and erythema are common side effects.

How hard is this question?

We tag it as an application question: it asks you to use a fact on a patient or a finding. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study Infections: bacterial, viral, fungal, parasitic: imiquimod in anogenital warts?

Learn each condition by its primary lesion, site and signature sign. Then use the flashcards and the other Dermatology questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.