Are the statements about Subacute Sclerosing Panencephalitis (SSPE) virus correct, specifically that it does not fully shut down antigen production, the measles viruses in SSPE are defective, and they express measles proteins leading to continuous antigen exposure?

SSPE Virus Antigen Production and Pathogenesis

The statements are essentially correct: SSPE measles viruses are defective mutants that continuously express viral proteins (particularly N, P, and mutated M fragments) without producing complete infectious virions, and this ongoing antigen exposure drives the persistent IgM response characteristic of SSPE. 1, 2, 3

Viral Defectiveness and Protein Expression

SSPE viruses are fundamentally defective, not dormant, characterized by their inability to produce infectious viral particles while maintaining protein expression. 3

• The virus exhibits biased hypermutation, most notably in the M gene, followed by F and H genes, which accounts for the defective phenotype 3
• Despite being unable to produce complete virions, SSPE viruses continue to express measles proteins including N (nucleoprotein), P (phosphoprotein), and mutated M (matrix) protein fragments 3
• Post-mortem brain tissue from SSPE patients shows abundant MeV RNA-positive cells throughout the brain, confirming continuous viral protein expression 2

Mechanism of Viral Spread Without Budding

• SSPE viruses establish true persistent infection in neurons and spread trans-synaptically rather than through normal budding mechanisms 1
• The hypermutated M gene results in defective matrix protein that cannot support normal viral assembly and budding 3
• Mutations in the F gene (particularly N465I) create a hyperfusogenic phenotype that allows cell-to-cell spread without requiring complete virion formation 2
• Recombinant MeV with SSPE-F genes efficiently disseminates in neural cultures through direct cell fusion rather than extracellular viral particles 2

Continuous Antigen Exposure and IgM Persistence

The ongoing expression of viral proteins provides continuous antigenic stimulation that maintains IgM production for years or decades, which is pathognomonic for SSPE. 1

• In acute measles, IgM becomes detectable 1-2 days after rash onset, peaks at 7-10 days, and becomes completely undetectable within 30-60 days 1
• In SSPE, measles-specific IgM remains persistently elevated in both serum and CSF (often higher in CSF) regardless of disease stage, reflecting ongoing immune stimulation from CNS viral replication 1
• The combination of persistent measles IgM in serum and CSF, elevated IgG, and CSF/serum measles antibody index ≥1.5 has 100% sensitivity and 93.3% specificity for SSPE diagnosis 1
• This persistent IgM is highly abnormal and distinguishes SSPE from acute measles infection, reinfection, or other neurological conditions 1

Clinical Implications

• The presence of persistent measles IgM years after potential measles exposure strongly suggests SSPE, not acute infection or reinfection 1
• Intrathecal synthesis of measles-specific antibodies (CSF/serum index ≥1.5) confirms local CNS production rather than systemic antibody leakage 1
• The isolated, extremely strong measles antibody response in SSPE should not be confused with the MRZ reaction in multiple sclerosis, which shows intrathecal synthesis against at least two of three viral agents 1

Prevention Remains Paramount

• Measles vaccination is the only effective prevention strategy for SSPE and has essentially eliminated the disease in highly vaccinated populations 4, 5
• The MMR vaccine does not increase SSPE risk, even among persons who previously had measles disease 1, 5