Interaction with host factors exacerbates Trypanosoma cruzi cell invasion capacity upon oral infection

Prehistoric earth oven facilities and the pathoecology of Chagas disease in the Lower Pecos Canyonlands

“…In the modern world, oral transmission of Chagas disease occurs when triatomines or triatomine feces are processed into food for human consumption (Covarrubias et al, 2007;Guhl et al, 2014). This potential is supported by experimental infections of mice (Hoft, 1996).…”

The role of adaptations in two-strain competition for sylvaticTrypanosoma cruzitransmission

“…Furthermore, it has been suggested that oral transmission of T. cruzi via host consumption of infected vectors (raccoons and opossums are both opportunistic feeders whose diets include insects) may be the dominant infection pathway in some cycles, more likely among raccoons than among opossums [32,37,40,49]. Oral transmission has also been documented in laboratory mice as well as in humans [4,7] and other primates [35]. Oral transmission is a risky adaptation in evolutionary terms since the consumed vector can infect at most one host this way, as opposed to potentially many via stercorarian transmission, but as shown in [24] it can, under some conditions, maintain sylvatic cycles alone.…”

Role of Δ1-Pyrroline-5-Carboxylate Dehydrogenase Supports Mitochondrial Metabolism and Host-Cell Invasion of Trypanosoma cruzi

“…humans) (2,4). Additionally, evidence of outbreaks attributed to vector-excreta-contaminated food indicates the oral transmission of T. cruzi (5,6). Recently, the World Health Organization warned that Chagas disease has become a more serious health problem due to its spread from endemic areas (south of the United States to Argentina and Chile) to nonendemic countries (3).…”

“…In CHO-K 1 cells, P5C was shown to be involved in redox metabolism by up-regulating the hexose monophosphate shunt pathway (33). Farrant et al (35) assessed the response of patients with P5CDH deficiency, which was previously reported as an inborn error of metabolism (hyperprolinemia type II), and showed that an increased intracellular P5C pool chemically inhibits vitamin B 6 (pyridoxal 5Ј-phosphate) (34), which is an essential prosthetic group of transaminases. Taken together, these data suggest that the proline-glutamate interconversion pathway participates in relevant physiological processes and that the altered equilibrium of their components might elicit detrimental effects beginning at the mitochondrial level and leading to cell death.…”

“…The K m value for the oxidation of ␥GS to L-Glu in the presence of TcP5CDH-His 6 Table 3). The enzymatic conversion was pH-dependent, and an optimal pH of 7.2 for either mitochondrial lysates or recombinant TcP5CDH-His 6 was determined (Fig.…”