Article Text
Abstract
Objectives To explore whether existence of long-lasting partial immunity against reinfection with Chlamydia trachomatis is necessary to explain C. trachomatis prevalence patterns by age and sexual risk, and to provide a plausible estimate for the effect size, defined here as a reduction in susceptibility to reinfection.
Methods A population-based mathematical model was constructed to describe C. trachomatis natural history and transmission dynamics by age and sexual risk. The model was parameterised using natural history, and epidemiological and sexual behaviour data, and applied for UK and US data. Sensitivity analyses were conducted to assess the robustness of predictions to variations in model structure and to examine the impact of alternative assumptions for the mechanism underlying partial immunity.
Results Partial immunity against reinfection was found necessary to explain observed C. trachomatis prevalence patterns by age and sexual risk. The reduction in susceptibility to reinfection was estimated at 93% using UK data (95% uncertainty interval (UI)=88%–97%) and at 67% using US data (95% UI=24%–88%). The model-structure sensitivity analyses affirmed model predictions. The immunity-mechanism sensitivity analyses suggested a mechanism of susceptibility reduction against reinfection or a mechanism of infectious-period duration reduction upon reinfection.
Conclusions A strong long-lasting partial immunity against C. trachomatis reinfection should be present to explain observed prevalence patterns. The mechanism of immunity could be either a reduction in susceptibility to reinfection or a reduction in duration of infection on reinfection. C. trachomatis infection appears to naturally elicit a strong long-lasting immune response, supporting the concept of vaccine development.
- sexually transmitted infection
- immunity
- epidemiology
- prevalence
- reinfection
- mathematical model.
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Footnotes
Handling editor Katy M E Turner
Contributors RO conceived the study, developed the mathematical models and conducted the analyses. HC contributed to data analysis and wrote the first draft of the article. CLA provided technical input. LJA-R led the study design and analyses. All authors contributed to results generation and interpretation and to writing of the article.
Funding RO acknowledges the support of Precursory Research for Embryonic Science and Technology (PRESTO) grant number JPMJPR15E1 from Japan Science and Technology Agency (JST), and Japan Society for the Promotion of Science (JSPS), Grant-in-Aid for Young Scientists (B) 15K19217. This publication was made possible by NPRP grant number 5-752-3-177 from the Qatar National Research Fund (a member of Qatar Foundation). The findings achieved herein are solely the responsibility of the authors.
Competing interests None declared.
Patient consent Not required.
Provenance and peer review Not commissioned; externally peer reviewed.
Data statement Model equations and parameters are provided in the online supplementary materials.