The Role of Acquired Immunity in the Spread of XXXX ): Explorations with a Microsimulation Model.

@entity1 @entity5 @entity1083 @entity281 @entity1799 @entity1082
BACKGROUND: Knowledge of the natural history of @entity1082 ), in particular the role of immunity, is crucial in estimating the (cost-) effectiveness of @entity5 screening strategies, because naturally acquired immunity after clearing an @entity281 may already protect part of the risk population against new @entity1083 . METHODS: We used STDSIM, an established stochastic microsimulation model, quantified to the Netherlands. We explored different assumptions regarding the natural history of @entity1799 and HPV-18, and estimated the transmission probabilities and durations of acquired immunity necessary to reproduce age-specific prevalence. RESULTS: A model without acquired immunity cannot reproduce the age-specific patterns of HPV. Also, it is necessary to assume a high degree of individual variation in the duration of @entity281 and acquired immunity. According to the model estimates, on average 20% of @entity1 are immune for @entity1799 and 15% for HPV-18. After an @entity1799 @entity281 , 50% are immune for less than 1 year, whereas 20% exceed 30 years. For HPV-18, up to 12% of the individuals are immune for less than 1 year, and about 50% over 30 years. Almost half of all @entity1 will never acquire @entity1799 or HPV-18. CONCLUSIONS: Acquired immunity likely plays a major role in HPV epidemiology, but its duration shows substantial variation. Combined with the lifetime risk, this explains to a large extent why many @entity1 will never develop @entity5 .
