HLA-C∗03 is a risk factor for cardiomyopathy in chagas disease

Layrisse, Z.; Fernández, Mercedes; Montagnani, S.; Matos, M.; Balbas, O.; Herrera, Flor; Colorado, Iriana; Catalioti, Franco; Acquatella, Harry

doi:10.1016/s0198-8859(00)00161-0

Cited by 42 publications

(30 citation statements)

References 15 publications

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“…The same finding was described in Mexicans with chronic Chagas' disease [79]. The diversity of these results is probably due to environmental influences, ethnic differences among the different groups, in addition to possible differences among the parasites that attack the various populations [69].…”

Section: Parasitic Infectionssupporting

confidence: 66%

“…In Venezuelans, a greater frequency of the HLA-C*03 allele was observed in patients with the cardiac form of Chagas' disease [69], and a low frequency of the HLA-DRB1*14 and -DQB1*0303 alleles was found in seropositive patients, inhabitants of an endemic region, suggesting the protective effect of these alleles against chronic infection [70]. Among seropositive patients, when comparing those with and without cardiomyopathy, high frequencies of the HLA-DRB1*01, -DRB1*08 and -DQB1*0501 alleles and low frequencies of-DRB1*1501 [69] were found in the cardiomyopathic group. Another study on this population in an endemic region revealed an association of the HLA-DRB1*01-DQB1*0501 haplotype with cardiomyopathy [71].…”

Section: Parasitic Infectionsmentioning

confidence: 99%

“…Thus, the HLA-DR4 and -B39 antigens may be associated with infection by T. cruzi; -DR16 with susceptibility to the cardiac condition, and -A68 with protection against cardiomyopathy [67]. In Venezuelans, a greater frequency of the HLA-C*03 allele was observed in patients with the cardiac form of Chagas' disease [69], and a low frequency of the HLA-DRB1*14 and -DQB1*0303 alleles was found in seropositive patients, inhabitants of an endemic region, suggesting the protective effect of these alleles against chronic infection [70]. Among seropositive patients, when comparing those with and without cardiomyopathy, high frequencies of the HLA-DRB1*01, -DRB1*08 and -DQB1*0501 alleles and low frequencies of-DRB1*1501 [69] were found in the cardiomyopathic group.…”

Section: Parasitic Infectionsmentioning

confidence: 99%

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Immunogenetics and infectious diseases: special reference to the mayor histocompatibility complex

Alves¹,

Souza²,

Meyer³

et al. 2006

Braz J Infect Dis

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Many studies have tried to identify genetic markers for infectious diseases, some of them have focused on human leukocyte antigens (HLA). The products of HLA genes interact with surfacespecific receptors of T lymphocytes, resulting in activation of the host's immune response. Association of bacterial, viral, parasitic and fungal infections with the host's HLA has been widely investigated. The type and strength of this association differs among distinct populations, as well as among racial and/or ethnic groups. The new molecular methods for the identification of the HLA alleles, and the resulting new nomenclature, have contributed to a better understanding of this system. Unfortunately, this information has not been adequately transmitted to clinicians, which hampers the understanding of the association between the HLA system and diseases. We revised relevant studies on the association of HLA genes with infectious diseases, demonstrating their importance in the pathogenic mechanisms, through increased susceptibility or protection against infections and their complications.

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Section: Parasitic Infectionssupporting

confidence: 66%

Section: Parasitic Infectionsmentioning

confidence: 99%

Section: Parasitic Infectionsmentioning

confidence: 99%

See 1 more Smart Citation

Immunogenetics and infectious diseases: special reference to the mayor histocompatibility complex

Alves¹,

Souza²,

Meyer³

et al. 2006

Braz J Infect Dis

View full text Add to dashboard Cite

show abstract

“…Associations were observed between distinct HLA alleles and an increased risk of developing chronic Chagas disease in some studies [49,50] , but others denied finding any such relationships [51] .…”

Section: From Acute To Chronic Chagas Diseasementioning

confidence: 99%

Chronic Chagas disease: from basics to laboratory medicine

Haberland

Saravia

Wallukat

et al. 2012

Clinical Chemistry and Laboratory Medicine (CCLM)

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Chagas disease, caused by Trypanosoma cruzi infection, is ranked as the most serious parasitic disease in Latin America and has huge potential to become a worldwide problem, due to increasing migration, and international tourism, as well as infectant transfer by blood contact and transfusion, intrauterine transfer, and organ transplantation. Nearly 30% of chronically-infected patients become symptomatic, often with a latency of 10–30 years, developing life-threatening complications. Of those, nearly 90% develop Chagas heart disease, while the others manifest gastrointestinal disease and neuronal disorders. Besides interrupting the infection cycle and chemotherapeutic infectant elimination, starting therapy early in symptomatic patients is important for counteracting the disease. This would be essentially supported by optimized patient management, involving risk assessment, early diagnosis and monitoring of the disease and its treatment. From economic and logistic viewpoints, the tools of laboratory medicine should be especially able to guarantee this. After summarizing the basics of chronic Chagas disease, such as the epidemiological data, the pathogenetic mechanisms thought to drive symptomatic Chagas disease and also treatment options, we present tools of laboratory medicine that address patient diagnosis, risk assessment for becoming symptomatic and guidance, focusing on autoantibody estimation for risk assessment and heart marker measurement for patient guidance. In addition, increases in levels of inflammation and oxidative stress markers in chronic Chagas disease are discussed.

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“…HLA-B40 and Cw3 combination was protective for CCC (Llop, et al, 1991), as resulted DRB1*14, DQB1*0303 (Fernandez-Mestre, et al, 1998), HLA-DQB1*06 (Deghaide, et al, 1998) and HLA-A68 (Cruz- Robles, et al, 2004). On the other hand, HLA-C*03 (Layrisse, et al, 2000), DRB1*1503 (Garcia Borras, et al, 2009) …”

Section: Genetic Factorsmentioning

confidence: 99%