# Unraveling the Mechanistic Links Between Species Diversity and Infection Risk From Zoonotic Pathogens With Direct Transmission Among Reservoir Hosts: Rodent‐Orthohantavirus Systems as Models

## TL;DR

This paper explores how species diversity affects infection risk from zoonotic pathogens, using rodent-hantavirus systems to explain the link between biodiversity loss and disease spread.

## Contribution

The paper proposes a mechanistic framework for understanding diversity-disease patterns in directly transmitted zoonotic systems.

## Key findings

- Host regulation is a key mechanism driving diversity-disease patterns in rodent-hantavirus systems.
- Other mechanisms have received less empirical support and attention.
- For a negative diversity-disease pattern, the primary host must be resilient to disturbance and vulnerable to competition or predation.

## Abstract

To explain patterns between anthropogenic loss of species diversity and the rise in the number of novel zoonotic diseases, the “dilution effect” hypothesis predicts that with lower species diversity, infection risk will increase. The underlying mechanisms have been largely investigated in systems where pathogen transmission is vector‐borne or environmental. Relatively less research has been conducted in systems where transmission is direct, such as with orthohantaviruses (hereafter hantaviruses) and their rodent reservoir hosts. These systems are commonly cited as supporting a negative diversity‐disease pattern. To motivate empirical research on underlying mechanisms driving this pattern, we extend a mechanistic framework that links species diversity and infection prevalence of directly transmitted zoonotic pathogens by using rodent‐hantavirus systems in the Americas as models. Additionally, we summarize empirical studies, synthesize mechanistic evidence, and identify knowledge gaps. Our findings suggest that host regulation is a key mechanism likely to drive diversity‐disease patterns in rodent‐hantavirus systems of the Americas. Other mechanisms have received less empirical support but also less attention. Although host regulation likely functions via density‐dependent transmission, and can thus change contact rates among hosts, consequences to other mechanisms have been neglected. As observed in rodent‐hantavirus systems in the Americas, we propose that for a negative diversity‐disease pattern to manifest, the primary reservoir host species should be resilient to anthropogenic disturbance but also vulnerable to competition, predation, or both, and the “diversity” measure should be associated with host density.

In this review, we synthesize mechanistic evidence for diversity‐disease patterns in rodent‐orthohantavirus systems in the Americas, models of directly transmitted disease systems. We found that host regulation has been examined the most while other mechanisms have received less attention. Based on our findings, we propose that for a negative diversity‐disease pattern to manifest, the primary reservoir host should be resilient to anthropogenic disturbance and vulnerable to competition, predation, or both, and the “diversity” measure should be associated with host density.