Distributed discrete-event simulation
ACM Computing Surveys (CSUR)
On Communicating Finite-State Machines
Journal of the ACM (JACM)
A brief history of cellular automata
ACM Computing Surveys (CSUR)
Theory of cellular automata: a survey
Theoretical Computer Science
Tutorial on agent-based modeling and simulation part 2: how to model with agents
Proceedings of the 38th conference on Winter simulation
Simulating Epstein-Barr virus infection with C-ImmSim
Bioinformatics
Book review: Wolfram's New Science: A New Start?
Artificial Intelligence
Encyclopedia of Complexity and Systems Science - v. 1-10
Encyclopedia of Complexity and Systems Science - v. 1-10
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Objective: This paper presents a conceptual model that is developed upon a characterization of human papillomavirus type 16 (HPV16) which is used to build a simulation prototype of the HPV16 growth process. Methodology: The human papillomavirus type 16 is the principal virus detected in invasive lesions of cervical cancer, and associated with the greater persistence and prevalence in pre-malignant and malignant lesions. The probability of acquiring an infection with HPV16 is extremely high in sexually active individuals. However, an HPV16 infection can disappear after becoming a histological confirmed case. According to the characterization of HPV16 proposed in this paper, cells as compared to a society behaves as a complex system, i.e., cells behave in a cooperative manner, following a set of rules defined by local interactions among them. Such complex system is defined by combining a cellular automaton and agent-based models. In this way, the behavior of the HPV16 is simulated by allowing the cellular automaton to follow such parameterized behavior rules. Results: Both cross-sectional and prospective studies indicate that HPV16 infection persistence increase the risk of high-grade CIN, as observed in the results provided by the growth simulation model of HPV16. The average growth rate extrapolated over 52 weeks (12 months) and calculated by the model showed a 37.87% growth for CIN1, 35.53% for CIN2 and 16.92% for CIN3. Remarkably, these results are similar to the results obtained and reported by clinical studies. For example, the results obtained using the proposed model for CIN2 and the results obtained by Ostor [36], have a differential of 0.53 percentage points while have a differential of 2.23 percentage points with the results obtained by Insinga et al. [51]. Also, for the CIN3, the results obtained using the proposed model, have a differential of 2.92 percentage points with the Insinga et al. [52], results. Conclusion: Through the specification of parameterized behavior rules for HPV16 that are simulated under the combined technique of cellular automata and agent-based models, the HPV life cycle can be simulated allowing for observations at different stages. The proposed model then can be used as a support tool in the investigation of HPV16, in particular (as part of our future work) to develop drugs as agents in the control of the HPV16 disease.