Comparison of Trypanosoma cruzi Lineages and Levels of Parasitic DNA in Infected Mothers and Their Newborns

Virreira, Myrna; Truyens, Carine; Alonso-Vega, Cristina; Brutus, Laurent; Jijena, Juan; Torrico, Faustino; Carlier, Yves; Svoboda, Michal

doi:10.4269/ajtmh.2007.77.102

Cited by 58 publications

(71 citation statements)

References 14 publications

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“…The parasite loads in women who transmitted infection, while higher than in nonpregnant adults with chronic T. cruzi infection, were substantially lower than those seen in the acute phase (eg, in congenitally infected infants) or in patients with human immunodeficiency virus (HIV) coinfection and T. cruzi reactivation [4,5]. HIV coinfection is also very unlikely to explain our findings.…”

contrasting

confidence: 46%

Reply to Henao-Martínez, et al

Bern

2015

Clin Infect Dis.

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contrasting

confidence: 46%

Reply to Henao-Martínez, et al

Bern

2015

Clin Infect Dis.

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“…The DTU TcV has been reported in 80-100% of congenital cases in Argentina, Bolivia, Southern Brazil, Chile, and Paraguay (Virreira et al, 2006a(Virreira et al, , 2007Burgos et al, 2007;Corrales et al, 2009;Diez et al, 2010;Bisio et al, 2011;Ortiz et al, 2012;Bua et al, 2013;Garcia et al, 2014;Llewellyn et al, 2015). DTUs TcII and TcVI have been reported in neonates from Argentina, Bolivia, Brazil (Bahia state) and Chile (Virreira et al, 2006a;Burgos et al, 2007;Ortiz et al, 2012;Garcia et al, 2014), whereas TcIII has been identified in Paraguay (del Puerto et al, 2010) and TcI in some neonates from Argentina, Chile and Colombia (Pavia et al, 2009;Ortiz et al, 2012;Bua et al, 2013).…”

Section: Parasite Diversity and Human Congenital Chagas Diseasementioning

confidence: 94%

“…The same T. cruzi DTUs are generally detected in mothers and their infected newborns, as well as in congenitally infected twins or siblings born in consecutive gestations (Burgos et al, 2007;Virreira et al, 2007). However, when multi-clonal infections occur with different DTUs or DTU variants (Virreira et al, 2006a;Burgos et al, 2007;Corrales et al, 2009;Bisio et al, 2011;Ortiz et al, 2012;Garcia et al, 2014;Llewellyn et al, 2015), slight differences can be observed between clones infecting mothers and those found in congenitally infected infants, suggesting that a natural selection of transmitted parasite populations might occur (Burgos et al, 2007;Ortiz et al, 2012;Llewellyn et al, 2015), perhaps through interactions with placental cells and/or the host immune system (see Section 5).…”

Section: Parasite Diversity and Human Congenital Chagas Diseasementioning

confidence: 99%

Congenital Chagas disease as an ecological model of interactions between Trypanosoma cruzi parasites, pregnant women, placenta and fetuses

2015

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The aim of this paper is to discuss the main ecological interactions between the parasite Trypanosoma cruzi and its hosts, the mother and the fetus, leading to the transmission and development of congenital Chagas disease. One or several infecting strains of T. cruzi (with specific features) interact with: (i) the immune system of a pregnant woman whom responses depend on genetic and environmental factors, (ii) the placenta harboring its own defenses, and, finally, (iii) the fetal immune system displaying responses also susceptible to be modulated by maternal and environmental factors, as well as his own genetic background which is different from her mother. The severity of congenital Chagas disease depends on the magnitude of such final responses. The paper is mainly based on human data, but integrates also complementary observations obtained in experimental infections. It also focuses on important gaps in our knowledge of this congenital infection, such as the role of parasite diversity vs host genetic factors, as well as that of the maternal and placental microbiomes and the microbiome acquisition by infant in the control of infection. Investigations on these topics are needed in order to improve the programs aiming to diagnose, manage and control congenital Chagas disease.

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“…Although the production of proinflammatory cytokines like IL-1b, IL-6, and TNF-a in response to T. cruzi Ags and the spontaneous release of TNF-a in uninfected infants born to T. cruzi-infected mothers (B 2 M + ) have been described, the levels of these cytokines in congenitally infected newborns are rather low (11,(13)(14)(15)(16), suggesting that the immune response might be an important factor in vertical transmission (17). By using a quantitative PCR (qPCR), we have previously demonstrated that the parasitemia of congenitally infected infants is highly variable at birth (7,18), and this fact posed the question whether T. cruzi-infected children also exhibit variable levels of chemokines and cytokines that might correlate with parasite burden and predict congenital infection. In this context, our study aimed to evaluate the chemokine and cytokine profiles in groups of congenitally infected and uninfected infants born to T. cruzi- Received for publication December 1, 2015.…”

mentioning

confidence: 99%

Serum Cytokines as Biomarkers of Early Trypanosoma cruzi infection by Congenital Exposure

Volta

Bustos

Cardoni

et al. 2016

The Journal of Immunology

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Trypanosoma cruzi, the causing agent of Chagas disease, leads to an activation of the immune system in congenitally infected infants. In this study, we measured a set of cytokines/chemokines and the levels of parasitemia by quantitative PCR in the circulation of neonates born to T. cruzi–infected mothers to evaluate the predictive value of these mediators as biomarkers of congenital transmission. We conducted a retrospective cohort study of 35 infants with congenital T. cruzi infection, of which 15 and 10 infants had been diagnosed by detection of parasites by microscopy in the first and sixth month after delivery, respectively, and the remaining 10 had been diagnosed by the presence of T. cruzi–specific Abs at 10–12 mo old. Uninfected infants born to either T. cruzi–infected or uninfected mothers were also evaluated as controls. The plasma levels of IL-17A, MCP-1, and monokine induced by IFN-γ were increased in infants congenitally infected with T. cruzi, even before they developed detectable parasitemia or seroconversion. Infants diagnosed between 6 and 12 mo old also showed increased levels of IL-6 and IL-17F at 1 mo of age. Conversely, infants who did not develop congenital T. cruzi infection had higher levels of IFN-γ than infected infants born to uninfected mothers. Monokine induced by IFN-γ, MCP-1, and IFN-γ production induced in T. cruzi–infected infants correlated with parasitemia, whereas the plasma levels of IL-17A, IL-17F, and IL-6 were less parasite load dependent. These findings support the existence of a distinct profile of cytokines and chemokines in the circulation of infants born to T. cruzi–infected mothers, which might predict congenital infection.

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Comparison of Trypanosoma cruzi Lineages and Levels of Parasitic DNA in Infected Mothers and Their Newborns

Cited by 58 publications

References 14 publications

Reply to Henao-Martínez, et al

Reply to Henao-Martínez, et al

Congenital Chagas disease as an ecological model of interactions between Trypanosoma cruzi parasites, pregnant women, placenta and fetuses

Serum Cytokines as Biomarkers of Early Trypanosoma cruzi infection by Congenital Exposure

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