Virology: measles complications: practice question

A Microbiology 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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Microbiology · Virology: measles complications

Sample item

A 9-year-old boy who had measles at 1 year of age develops progressive intellectual deterioration, school failure and myoclonic jerks over 6 months. EEG shows periodic high-voltage complexes and CSF has very high anti-measles antibody titres. What is the underlying mechanism?

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

The answer and the reasoning

C. Persistence of defective measles virus in neurons

Subacute sclerosing panencephalitis follows early childhood measles after a latent period of several years. Mutant measles virus with defective matrix protein persists in neurons and spreads cell to cell, producing inflammation and gliosis. Measles vaccination prevents it.

Option by option

  • A. Reactivation of latent varicella-zoster virus in dorsal root ganglia

    Varicella-zoster reactivation causes dermatomal zoster rather than a progressive dementia with measles antibodies.

  • B. Replication of JC polyomavirus in oligodendrocytes

    JC virus causes progressive multifocal leukoencephalopathy in immunosuppressed adults, not in a child with CSF measles antibody.

  • C. Persistence of defective measles virus in neurons (correct)

    Correct. Defective measles virus persisting in neurons explains subacute sclerosing panencephalitis.

  • D. Accumulation of misfolded prion protein in the cortex

    Prion disease would not produce high CSF anti-measles antibody titres.

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 Microbiology question

What is the answer to this Microbiology question?

The best answer is C, Persistence of defective measles virus in neurons. Subacute sclerosing panencephalitis follows early childhood measles after a latent period of several years.

Why is "Reactivation of latent varicella-zoster virus in dorsal root ganglia" not the answer?

Varicella-zoster reactivation causes dermatomal zoster rather than a progressive dementia with measles antibodies.

Why is "Replication of JC polyomavirus in oligodendrocytes" not the answer?

JC virus causes progressive multifocal leukoencephalopathy in immunosuppressed adults, not in a child with CSF measles antibody.

Why is "Accumulation of misfolded prion protein in the cortex" not the answer?

Prion disease would not produce high CSF anti-measles antibody titres.

What concept does this question test?

It tests Virology: measles complications in Microbiology. Mutant measles virus with defective matrix protein persists in neurons and spreads cell to cell, producing inflammation and gliosis. Measles vaccination prevents it.

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 Virology: measles complications?

Make a one-line identity card for each organism: shape and stain, defining test, toxin, disease and drug. Then use the flashcards and the other Microbiology 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.