Can Triatoma virus inhibit infection of Trypanosoma cruzi (Chagas, 1909) in Triatoma infestans (Klug)? A cross infection and co-infection study

MARTI, GERARDO ANÍBAL; BALSALOBRE, AGUSTÍN; CECCARELLI, SOLEDAD; DIOSQUE, PATRICIO; ECHEVERRÍA, MARÍA GABRIELA; MARTI, GERARDO ANÍBAL; RAGONE, PAULA; CECCARELLI, SOLEDAD; SUSEVICH, MARÍA LAURA; ECHEVERRÍA, MARÍA GABRIELA; RABINOVICH, JORGE EDUARDO; RAGONE, PAULA; SUSEVICH, MARÍA LAURA; RABINOVICH, JORGE EDUARDO; BALSALOBRE, AGUSTÍN; DIOSQUE, PATRICIO

JOURNAL OF INVERTEBRATE PATHOLOGY

ACADEMIC PRESS INC ELSEVIER SCIENCE

Año: 2017 vol. 150 p. 101 - 105

0022-2011

Triatoma virus occurs infecting Triatominae in the wild (Argentina) and in insectaries (Brazil). Pathogenicity of Triatoma virus has been demonstrated in laboratory; accidental infections in insectaries produce high insect mortality. When more than one microorganism enters the same host, the biological interaction among them differs greatly depending on the nature and the infection order of the co-existing species of microorganisms. We studied the possible interactions between Triatoma virus (TrV) and Trypanosoma cruzi (the etiological agent of Chagas disease) in three different situations: (i) when Triatoma virus is inoculated into an insect host (Triatoma infestans) previously infected with T. cruzi, (ii) when T. cruzi is inoculated into T. infestans previously infected with TrV, and (iii) when TrV and T. cruzi are inoculated simultaneously into the same T. infestans individual. Trypanosoma cruzi infection was found in 57% of insects in the control group for T. cruzi, whereas 85% of insects with previous TrV infection were infected with T. cruzi. TrV infection was found in 78.7% of insects in the control group for TrV, whereas insects previously infected with T. cruzi showed 90% infection with TrV. A total of 67.9% of insects presented simultaneous infection with both types of microorganism. Our results suggest that TrV infection could increase adhesion of T. cruzi to the intestinal cells of triatomines, but presence of T. cruzi in intestinal cells would not increase the possibility of entry of TrV into cells. Although this study cannot explain the mechanism through which TrV facilitates the infection of triatomines with T. cruzi, we conclude that after TrV replication, changes at cellular level should occur that increase the adhesion of T. cruzi.