HIV and Chagas Disease Coinfection, a Tractable Disease?

Guidetto, B.; Tatta, Melisa; Latini, V.; Gonzales, Milene; Riarte, Adelina; Tavella, Silvina; Warley, Eduardo; Altclas, Javier

doi:10.1093/ofid/ofz307

Cited by 7 publications

(4 citation statements)

References 9 publications

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“…In these cases, the diagnosis needs to be actively searched since a better response to antiparasitic treatment has been shown in severe cases [ 5 , 15 , 21 , 23 ].…”

Section: Discussionmentioning

confidence: 99%

“…Co-infection cases have been reported predominantly in Brazil and Argentina, but also in Spain, USA, Chile, Colombia, Jamaica, Germany, Switzerland, Bolivia, Venezuela [ 5 , 7 , 12 – 23 ]. The prevalence of co-infection is estimated at 1.3%-2.3% in São Paulo State [ 5 , 24 ] and 5.0% in Rio Grande do Sul State [ 25 ] in Brazil and 4.2% in Argentina, varying from 1.3 to 10.5% in endemic areas [ 5 , 21 , 24 – 26 ] and in a restricted group of HIV infected immigrants from CD endemic areas [ 27 ], with higher rates in drug users in Argentina [ 21 , 26 ].…”

Section: Introductionmentioning

confidence: 99%

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Clinical profile and mortality in patients with T. cruzi/HIV co-infection from the multicenter data base of the “Network for healthcare and study of Trypanosoma cruzi/HIV co-infection and other immunosuppression conditions”

et al. 2021

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Objective Chagas disease (CD) globalization facilitated the co-infection with Human Immunodeficiency Virus (HIV) in endemic and non-endemic areas. Considering the underestimation of Trypanosoma cruzi (T. cruzi)-HIV co-infection and the risk of life-threatening Chagas Disease Reactivation (CDR), this study aimed to analyze the major co-infection clinical characteristics and its mortality rates. Methods This is a cross-sectional retrospective multicenter study of patients with CD confirmed by two serological or one parasitological tests, and HIV infection confirmed by immunoblot. CDR was diagnosed by direct microscopy with detection of trypomastigote forms in the blood or other biological fluids and/or amastigote forms in inflammatory lesions. Results Out of 241 patients with co-infection, 86.7% were from Brazil, 47.5% had <200 CD4+ T cells/μL and median viral load was 17,000 copies/μL. Sixty CDR cases were observed. Death was more frequent in patients with reactivation and was mainly caused by CDR. Other causes of death unrelated to CDR were the manifestation of opportunistic infections in those with Acquired Immunodeficiency Syndrome. The time between the co-infection diagnosis to death was shorter in patients with CDR. Lower CD4+ cells count at co-infection diagnosis was independently associated with reactivation. Similarly, lower CD4+ cells numbers at co-infection diagnosis and male sex were associated with higher lethality in CDR. Additionally, CD4+ cells were lower in meningoencephalitis than in myocarditis and milder forms. Conclusion This study showed major features on T. cruzi-HIV co-infection and highlighted the prognostic role of CD4+ cells for reactivation and mortality. Since lethality was high in meningoencephalitis and all untreated patients died shortly after the diagnosis, early diagnosis, immediate antiparasitic treatment, patient follow-up and epidemiological surveillance are essentials in T. cruzi/HIV co-infection and CDR managements.

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“…In these cases, the diagnosis needs to be actively searched since a better response to antiparasitic treatment has been shown in severe cases [ 5 , 15 , 21 , 23 ].…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Clinical profile and mortality in patients with T. cruzi/HIV co-infection from the multicenter data base of the “Network for healthcare and study of Trypanosoma cruzi/HIV co-infection and other immunosuppression conditions”

et al. 2021

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“…Moreover, this evidence supports that the progression of T. cruzi infection is related to a decline in the immune T cell response and parasite persistence. This above mentioned is supported by evidence of the scientific literature, as follows: i) chagasic patients coinfected with HIV/AIDS with low CD4 + T cell counts exhibited reactivation of T. cruzi infection, which results in high mortality due to severe complications in the central nervous system and myocardium ( Martins-Melo et al., 2012 ; Guidetto et al., 2019 ); ii) an increased number of T. cruzi -infected individuals under immunosuppressive therapy present reactivation of the infection with detectable parasitemia in the blood ( Campos et al., 2008 ; da Costa et al., 2017 ); iii) repeated infections increase the risk of progression to the symptomatic stage in developing cardiomyopathy ( Bustamante et al., 2002 ; Basquiera et al., 2003 ; Bustamante et al., 2007 ); and iv), the administration of therapy based on antiparasitic drugs to asymptomatic patients with ChD prevents the occurrence of electrocardiographic alterations ( Fragata-Filho et al., 2016 ). However, the direct relationship between the immune response and parasite persistence has not been established.…”

Section: Discussionmentioning

confidence: 66%

CD8+ T Cell Response Quality Is Related to Parasite Control in an Animal Model of Single and Mixed Chronic Trypanosoma cruzi Infections

Mateus

Nocua

Lasso

et al. 2021

Front. Cell. Infect. Microbiol.

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Chagas disease (ChD) is a chronic infection caused by Trypanosoma cruzi. This highly diverse intracellular parasite is classified into seven genotypes or discrete typing units (DTUs) and they overlap in geographic ranges, vectors, and clinical characteristics. Although studies have suggested that ChD progression is due to a decline in the immune response quality, a direct relationship between T cell responses and disease outcome is still unclear. To investigate the relationship between parasite control and immune T cell responses, we used two distinct infection approaches in an animal model to explore the histological and parasitological outcomes and dissect the T cell responses in T. cruzi-infected mice. First, we performed single infection experiments with DA (TcI) or Y (TcII) T. cruzi strains to compare the infection outcomes and evaluate its relationship with the T cell response. Second, because infections with diverse T. cruzi genotypes can occur in naturally infected individuals, mice were infected with the Y or DA strain and subsequently reinfected with the Y strain. We found different infection outcomes in the two infection approaches used. The single chronic infection showed differences in the inflammatory infiltrate level, while mixed chronic infection by different T. cruzi DTUs showed dissimilarities in the parasite loads. Chronically infected mice with a low inflammatory infiltrate (DA-infected mice) or low parasitemia and parasitism (Y/Y-infected mice) showed increases in early-differentiated CD8+ T cells, a multifunctional T cell response and lower expression of inhibitory receptors on CD8+ T cells. In contrast, infected mice with a high inflammatory infiltrate (Y-infected mice) or high parasitemia and parasitism (DA/Y-infected mice) showed a CD8+ T cell response distinguished by an increase in late-differentiated cells, a monofunctional response, and enhanced expression of inhibitory receptors. Overall, our results demonstrated that the infection outcomes caused by single or mixed T. cruzi infection with different genotypes induce a differential immune CD8+ T cell response quality. These findings suggest that the CD8+ T cell response might dictate differences in the infection outcomes at the chronic T. cruzi stage. This study shows that the T cell response quality is related to parasite control during chronic T. cruzi infection.

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“…Secondary prophylaxis for PWH treated for T. cruzi infection is often recommended in countries with relatively high T. cruzi prevalence [ 73 ]. In one Argentine case series, after initial treatment for T. cruzi CNS reactivation disease, two PWH were successfully treated with benznidazole secondary prophylaxis at 5 mg/kg/d for three days a week until achieving CD4 counts higher than 200 cells/mm 3 and an undetectable HIV viral load [ 83 ].…”

Section: Treatmentmentioning

confidence: 99%

Chagas Disease in People with HIV: A Narrative Review

Clark

Bern

2021

TropicalMed

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Many questions remain unanswered regarding the epidemiology, pathophysiology, diagnosis, treatment, and monitoring of Trypanosoma cruzi infection in people with HIV (PWH). The reported prevalence of T. cruzi infection in PWH living in endemic countries ranges from 1–28% and is likely similar in at-risk US populations. While classic cardiac and gastrointestinal presentations of chronic Chagas disease occur in PWH, PWH are additionally at risk for a severe and often fatal form of T. cruzi-mediated disease called reactivation disease. T. cruzi reactivation typically occurs in PWH with low CD4 counts and poor virologic control. National HIV guidelines in several endemic South American countries recommend that all PWH be screened for T. cruzi infection at the time of HIV diagnosis; however, this recommendation is not widely implemented. The early detection of T. cruzi infection in PWH is critical as the sequelae of Chagas disease, including T. cruzi reactivation, may be preventable through the restoration of robust cellular immunity via the initiation of antiretroviral therapy and the appropriate use of antitrypanosomal therapy.

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HIV and Chagas Disease Coinfection, a Tractable Disease?

Cited by 7 publications

References 9 publications

Clinical profile and mortality in patients with T. cruzi/HIV co-infection from the multicenter data base of the “Network for healthcare and study of Trypanosoma cruzi/HIV co-infection and other immunosuppression conditions”

Clinical profile and mortality in patients with T. cruzi/HIV co-infection from the multicenter data base of the “Network for healthcare and study of Trypanosoma cruzi/HIV co-infection and other immunosuppression conditions”

CD8+ T Cell Response Quality Is Related to Parasite Control in an Animal Model of Single and Mixed Chronic Trypanosoma cruzi Infections

Chagas Disease in People with HIV: A Narrative Review

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