# Rhodnius prolixus Viruses Interfere with Proliferation and Metacyclogenesis of the Chagas Disease Agent Trypanosoma cruzi

## TL;DR

This study explores how viruses in Rhodnius prolixus insects may interfere with the development of the Chagas disease parasite, Trypanosoma cruzi.

## Contribution

The study reveals a novel interaction between insect viruses and T. cruzi, suggesting a potential role for viruses in controlling parasite development.

## Key findings

- Rhodnius prolixus viruses can infect the gut of the insect and interact with T. cruzi.
- Infection with RpVs reduces the proliferation and differentiation of T. cruzi in vitro.
- Viral genomes from RpV1 are detectable in the cytoplasm of T. cruzi.

## Abstract

The protozoan Trypanosoma cruzi is the etiological agent of Chagas disease, a neglected tropical disease that mostly affects the population of Latin American countries, with an estimated 7 million infected people and more than 10,000 deaths per year worldwide. T. cruzi is typically transmitted by hematophagous triatomine insects, with Rhodnius prolixus being a major insect vector in South America. While the microbiome of triatomine insects has been investigated to a certain extent, the ternary interaction between triatomes insects, T. cruzi, and viruses remains virtually unexplored. In this study, we show by transmission electron microscopy and by RT-PCR that Rhodnius prolixus viruses (RpVs) can infect the intestine of R. prolixus, which places them in close contact with the gut microbiota. These observations suggest that T. cruzi can be infected by the insect viruses while transiting through the gut. Here, we show that the RpVs are capable of infecting the epimastigote forms of T. cruzi in vitro and maintain the viral load stabilized for 3 to 7 days after infection. We also show that, at least in the case of the iFlavirus RpV1, viral genomes are detectable in the T. cruzi cytoplasm. Interestingly, R. prolixus ovarian extracts enriched with RpVs decrease epimastigote proliferation and their capacity for differentiation into the ineffective metacyclic trypomastigotes in vitro. Our results start to shed light on the interaction between RpVs and T. cruzi, suggesting possible routes of infection and unveiling a role for viral infections in the development of this important pathogen.