Modeling the Dynamics of Human Papillomavirus to Inform Vaccination Strategy
Modeling the Dynamics of Human Papillomavirus to Inform Vaccination Strategy
批准号:
9258929
负责人:
Sylvia Ranjeva
金额:
$4.9万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2017
资助国家:
美国
项目状态:
已结题
起止时间:
2017-01-01 至 2019-12-31
关键词:
AddressAffectAnogenital venereal wartsAutomobile DrivingBehavior TherapyBehavioralBiologicalDataDatabasesDemographic FactorsEcologyEpidemiologyHeterogeneityHumanHuman Papilloma Virus VaccinationHuman Papilloma Virus VaccineHuman PapillomavirusHuman papilloma virus infectionImmuneImmunityIndividualInfectionInterventionKnowledgeLeadMalignant NeoplasmsMalignant neoplasm of cervix uteriMarkov ChainsMarkov chain Monte Carlo methodologyMeasuresModelingNonlinear DynamicsOncogenicPatientsPopulationPredispositionPrevalencePublic HealthResearchRiskRisk FactorsRoleSamplingSeriesSexually Transmitted DiseasesShapesStreptococcus pneumoniaeTestingTimeUncertaintyVaccinationVaccinesVariantViralWeightWomanWorkbasebehavioral healthco-infectiondemographicsexperimental studyhigh riskhuman diseaselongitudinal datasetmalignant oropharynx neoplasmmathematical modelmennetwork modelspathogenpublic health interventionsexually activesimulationsocialtraittransmission processvaccination strategy
中文摘要
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英文摘要
Abstract
Despite the public health burden posed by human papillomavirus (HPV) - associated cancers, it is unclear how
social and behavioral traits, different kinds of host immunity, and competition between types shape the
epidemiology of HPV. The individual-level risk factors that sustain HPV, which may differ between HPV types,
define high-risk subpopulations that are key to behavioral public health interventions. Biological interactions
between HPV types, which may be synergistic, neutral, or competitive, determine the effect of HPV vaccines.
The eradication of vaccine-targeted types could lead to “type replacement” by competing non-targeted types, a
phenomenon that has been observed in pneumococcus. The proposed project investigates these aspects of
HPV ecology and epidemiology by fitting mechanistic mathematical models to longitudinal data. The data span
37 different HPV types in over 4,000 men sampled across nine years at six-month intervals. The data contain
information about patient demographics and sexual practices that affect viral dynamics. By fitting a mechanistic
transmission model, we will measure how different behavioral and health traits affect susceptibility to infection
and identify core risk groups that may sustain transmission in the population. Furthermore, we will infer the
degree and timescale of HPV interactions. We will measure the impact of previous infections on HPV dynamics
to infer the extent and duration of immunity in natural infection. We will also measure the impact of coinfections
to infer how types interact directly. Our approach, based on Markov Chain Monte Carlo methods for Partially
Observed Markov Processes, implicitly incorporates the stochastic, nonlinear dynamics of infection. The
proposed research will, for each HPV type, measure its transmissibility in different subpopulations, interactions
with other types, and interactions with host immunity. This information will be used in contact network
simulations to predict the consequences of current and hypothetical eradication efforts and to optimize
intervention strategies.
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