Trypanosoma cruzi (Chagas' disease agent) reduces HIV-1 replication in human placenta

Dolcini, Guillermina Laura; Solana, María Elisa; Andreani, Guadalupe; Celentano, Ana M.; Parodi, Laura M.; Donato, Ana Maria; Elissondo, Natalia; Cappa, S. M. González; Giavedoni, Luis D.; Peralta, Liliana Martínez

doi:10.1186/1742-4690-5-53

Cited by 20 publications

(17 citation statements)

References 59 publications

(56 reference statements)

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“…In this regard, it has been shown that IL-6, IL-8, IP-10 and MCP-1, which downmodulate T. cruzi replication [22], are diminished in human placental histocultures co-infected with HIV and T. cruzi, as well as in those stimulated with parasite-shed/-secreted factors. However, T. cruzi inhibits HIV replication at the placental level [23]. Similar results were observed in primary human monocyte-derived macrophages (MDMs), where HIV replication was inhibited by both free trypomastigotes and trypomastigote soluble factors.…”

Section: Key Pointssupporting

confidence: 55%

Mechanisms of interaction between protozoan parasites and HIV

Andreani

Lodge

Richard

et al. 2012

Current Opinion in HIV and AIDS

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Section: Key Pointssupporting

confidence: 55%

Mechanisms of interaction between protozoan parasites and HIV

Andreani

Lodge

Richard

et al. 2012

Current Opinion in HIV and AIDS

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“…We recently reported that T. cruzi inhibited HIV replication in human chorionic villi histocultures and in a trophoblast cell line. The study suggested that coinfection with T. cruzi may have a deleterious effect on HIV-1 transduction and thus, it could play an important role in viral outcome at the placental level [26]. Here, we have conducted studies of HIV/ T. cruzi co-infection in their common cellular target: human macrophages.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of HIV-1 Replication in Human Monocyte-Derived Macrophages by Parasite Trypanosoma cruzi

et al. 2009

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BackgroundCells of monocyte/macrophage lineage are one of the major targets of HIV-1 infection and serve as reservoirs for viral persistence in vivo. These cells are also the target of the protozoa Trypanosoma cruzi, the causative agent of Chagas disease, being one of the most important endemic protozoonoses in Latin America. It has been demonstrated in vitro that co-infection with other pathogens can modulate HIV replication. However, no studies at cellular level have suggested an interaction between T. cruzi and HIV-1 to date.Methodology/Principal FindingsBy using a fully replicative wild-type virus, our study showed that T. cruzi inhibits HIV-1 antigen production by nearly 100% (p<0.001) in monocyte-derived macrophages (MDM). In different infection schemes with luciferase-reporter VSV-G or BaL pseudotyped HIV-1 and trypomastigotes, T. cruzi induced a significant reduction of luciferase level for both pseudotypes in all the infection schemes (p<0.001), T. cruzi-HIV (>99%) being stronger than HIV-T. cruzi (∼90% for BaL and ∼85% for VSV-G) infection. In MDM with established HIV-1 infection, T. cruzi significantly inhibited luciferate activity (p<0.01). By quantifying R-U5 and U5-gag transcripts by real time PCR, our study showed the expression of both transcripts significantly diminished in the presence of trypomastigotes (p<0.05). Thus, T. cruzi inhibits viral post-integration steps, early post-entry steps and entry into MDM. Trypomastigotes also caused a ∼60-70% decrease of surface CCR5 expression on MDM. Multiplication of T. cruzi inside the MDM does not seem to be required for inhibiting HIV-1 replication since soluble factors secreted by trypomastigotes have shown similar effects. Moreover, the major parasite antigen cruzipain, which is secreted by the trypomastigote form, was able to inhibit viral production in MDM over 90% (p<0.01).Conclusions/SignificanceOur study showed that T. cruzi inhibits HIV-1 replication at several replication stages in macrophages, a major cell target for both pathogens.

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“…The role of such microbiota on the transmission of congenital infection, and more specifically the role of its bacterial composition on the capacity of T. cruzi to infect placental cells (trophoblast, fibroblasts, Hofbauer-, smooth muscle-, amniotic-and endothelial-cells) deserve further investigations. In connection with this new potential ecological association with congenital Chagas disease, it is of interest to note that previous observations reported that T. cruzi reduces HIV-1 replication in human placenta (Dolcini et al, 2008).…”

Section: Interpretation Attempt Of T Cruzi-placenta Interactionsmentioning

confidence: 98%

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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Trypanosoma cruzi (Chagas' disease agent) reduces HIV-1 replication in human placenta

Cited by 20 publications

References 59 publications

Mechanisms of interaction between protozoan parasites and HIV

Mechanisms of interaction between protozoan parasites and HIV

Inhibition of HIV-1 Replication in Human Monocyte-Derived Macrophages by Parasite Trypanosoma cruzi

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

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