A 14-year-old boy develops insidious intellectual decline, myoclonic jerks, and generalized seizures over one year. EEG shows periodic complexes, and CSF contains markedly elevated anti-measles antibodies with normal glucose and mild pleocytosis. He had uncomplicated measles at age 4. The underlying defect in the causative agent involves:

• A Loss of the matrix (M) protein, producing defective non-productive virions that persist in neurons ✓
• B Acquisition of a neuraminidase gene from avian influenza by reassortment
• C Mutation of the hemagglutinin gene conferring antibody escape
• D Integration of the entire viral genome into the host chromosome as proviral DNA

Explanation

Subacute sclerosing panencephalitis is a rare late sequela of measles, appearing 5 to 10 years after the initial infection. The CNS harbours defective measles virus that expresses nucleocapsid antigens abundantly but lacks functional M (matrix) protein, so infectious virions cannot be assembled and released, allowing persistent intracellular infection. Measles is an RNA virus that never integrates into host DNA, and reassortment applies to segmented influenza genomes.

Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.