# Disentangling the role of parasite infectivity and density from host susceptibility in infection development and parasite proliferation

## TL;DR

This study explores how parasite infectivity and host susceptibility influence infection outcomes, using a controlled host-parasite system.

## Contribution

The research disentangles the effects of parasite infectivity and host susceptibility in a matching-allele system.

## Key findings

- Parasite isolates showed significant differences in infectivity and proliferation rate after controlling for exposure and host genotype.
- Host susceptibility strongly influenced infection success and parasite proliferation.
- Exposure dose did not affect infection numbers or intensity, and no covariance was found between infection success and proliferation rate.

## Abstract

Understanding the environmental drivers of host–parasite interactions is a major concern to human health and conservation, particularly in the context of emerging infectious diseases. The likelihood of contracting an infection can be related to both the rate of contact between host and parasite, as well as innate features of hosts (susceptibility/resistance) and parasites (infectivity, virulence, within-host proliferation rate). This study uses a host–parasite system with a matching-allele model for host susceptibility and parasite infectivity to disentangle contact rate from parasite infectivity while accounting for the effects of host susceptibility. Using three exposure doses from several parasite isolates to hosts with known susceptibility, we find significant differences in parasite infectivity (in terms of number of successful infections) and within-host proliferation rate among parasite isolates, after controlling for exposure rate and host genotype. Host known susceptibility also had a strong impact on parasite infection success and proliferation rate, due to the nature of this host–parasite system. The exposure dose did not impact the number of infections or infection intensity. No significant relationship between infection success and parasite proliferation rate was detected, indicating a weak or non-existent covariance among isolates for both variables.