Modelling Within-Host Immune Response to Visceral Helminthiasis and Malaria Co-infection with Prophylaxis

TL;DR

This paper models the within-host immune response to co-infection of malaria and visceral helminthiasis, analyzing stability and thresholds for infection dynamics with and without immune response.

Contribution

It introduces a mathematical model capturing immune interactions and thresholds in malaria and helminth co-infection within hosts, including immune response effects.

Findings

Identifies conditions for stable and unstable infection states.

Shows immune response delays until certain immunological thresholds are exceeded.

Highlights threshold drug action levels for recovery.

Abstract

In this paper, a co-infection of malaria and visceral helminthiasis with immune stimulation and impairment is studied. We have assumed that an individual gets malaria infection during invasion by helminths larvae. In absence of immune response, our results show that the antigens invade the blood system if the rate of red cell rupture per invading merozoite is greater than one. If fewer merozoites are released, the initial state is globally asymptotically stable. If more merozoites are released, there exists malaria-only endemic point. However, both antigens coexist if the mean infection burden is greater than one. In this case, there is a threshold value for drug action below which no recovery of host is expected. In presence of immune response, three equilibrium states exist. The initial invasion state, and secondly, the unstable state when the immune population has been triggered and the antigens have been eliminated. The third state represents the endemic state which is stable if the infection-induced rupture rate per erythrocyte with immune activation is less than the total mortality of the erythrocytes. A model for severity of the co-infection shows that an immune response will be delayed until immunological barrier values for malaria and helminths are exceeded.