Models of superinfection and acquired immunity to multiple parasite strains

Abstract

Individuals in communities in which different strains of pathogen are circulating can acquire resistance by accumulating immunity to each strain. After considering susceptibility, models of infection and immunity are defined for vector-borne diseases such as malaria and trypanosomiasis. For these models the prevalence of infection, the number of infections per individual, and the mean duration of infection, increase rapidly in young individuals, but decrease in older individuals as immunity is acquired to the various strains of pathogen; the mean interval between successive infections lengthens with age. The bivariate Poisson distribution is shown to be a close approximation to some stochastic processes. The models explain observed cross-sectional patterns of age prevalence, and longitudinal patterns in which individuals typically continue to become infected as they age, albeit with decreasing frequency. In these models the time spent infected depends on parasite diversity, as well as the inoculation and recovery rates. It is shown that control measures can cause an increase in the number of infections and the prevalence of infection in older individuals, and in the average prevalence in the community, even when strain-specific immunity is life-long.

A mathematical model of seropositivity to malaria antigen, allowing seropositivity to be prolonged by exposure

“…For example, Nasell has shown that young children may experience superinfection up to age 5 but it is not common in adults [10]. In a multistrain model, Milligan and Downham found similar conclusions that the fraction of infection increased more rapidly in younger children than in adults as they acquire immunity to different strains of pathogens [9]. In a recent study, Portugal and colleagues held an opposite view that superinfections are uncommon in younger children [20].…”

A simple agent-based model of malaria transmission investigating intervention methods and acquired immunity

“…Acquired immunity. Acquired immunity is gained through repeated exposure to the malaria parasite, and the effects of acquired immunity have been previously modeled [Aron 1983;Chiyaka et al 2007;Gu et al 2003;Gurarie and McKenzie 2007;Milligan and Downham 1996;Tumwiine et al 2007]. Previous models have considered acquired immunity as leading to milder forms of the disease [Tumwiine et al 2007] and have defined acquired immunity in a host as protection against severe illness [Chiyaka et al 2007].…”

“…In modeling the spread of acquired immunity in the current ABM, human agents were assumed to gain immunity after a certain number of infections as in [Milligan and Downham 1996]. Once a host has reached a certain level of infections, the host was assumed to lose immunity at a particular rate (if not reinfected) [ 1983; Milligan and Downham 1996]. Gu et al [2003] investigated an ABM with acquired immunity, but their model did not incorporate latency and did allow for superinfection.…”