Measles Genotype and SSPE Risk
Current evidence does not support that specific measles genotypes confer differential risk for developing SSPE—the primary determinant of SSPE risk is measles infection itself, particularly when contracted before age 5 years, not the viral genotype. 1, 2
Evidence on Genotype-Specific Risk
The available evidence does not demonstrate genotype-specific predisposition to SSPE development:
Genotype analysis from SSPE cases confirms measles virus identity but does not reveal specific genotypes that preferentially cause SSPE. When brain tissue from 11 SSPE patients was analyzed by RT-PCR and sequencing, the focus was on confirming measles virus and linking cases to the 1989-1991 U.S. measles resurgence, not on identifying high-risk genotypes 3
The mutations that characterize SSPE virus occur after initial infection within the CNS, not as pre-existing genotype characteristics. Measles virus recovered from autopsied brain tissue shows clustered mutations particularly in the M gene that destroy protein structure and function, with F protein mutations conferring hyperfusogenic properties for transneuronal spread—these are acquired mutations during persistent CNS infection, not inherent genotype features 4
What Actually Determines SSPE Risk
The established risk factors are independent of viral genotype:
Age at measles infection is the dominant risk factor: SSPE occurs in 4-11 per 100,000 measles cases overall, but risk increases to 18 per 100,000 when measles is contracted under 1 year of age 1, 5
Immunocompromised states increase risk: HIV infection or other immunocompromising conditions that increase susceptibility to severe measles also elevate SSPE risk 6, 2
Lack of vaccination is the primary modifiable risk factor: The only effective prevention remains measles vaccination, which has essentially eliminated SSPE in highly vaccinated populations 1, 7
Clinical Implications
Do not stratify SSPE risk based on presumed infecting genotype—focus prevention efforts on universal measles vaccination regardless of circulating genotype 1
The 10-fold higher SSPE risk identified after the 1989-1991 U.S. measles resurgence (compared to 1982 estimates) reflects increased case ascertainment and younger age at infection, not genotype virulence 3
Genetic predisposition refers to host factors, not viral genotype—WHO emphasizes that no measles infection means no SSPE regardless of genetic profile 1