Possible integration of Trypanosoma cruzi kDNA minicircles into the host cell genome by infection

Teixeira, Antonio R. L.; Argañaraz, Enrique R.; Freitas, Lucio H.G de; Lacava, Z.G.M.; Santana, Jaime M.; Luna, Helena

doi:10.1016/0027-5107(94)90240-2

Cited by 42 publications

(43 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Since the parasite nuclear DNA does not integrate in the host DNA, the presence of PCR amplification product with T. cruzi nuclear DNA PON1/PON2 was considered evidence of a living infection. 29 Furthermore, the evidence of ongoing infections is in keeping with immunological test results, which were indistinguishable in treated and untreated groups of patients.…”

Section: Discussionsupporting

confidence: 55%

“…We conducted PCR with T. cruzi nuclear DNA specific set of primers to monitor drug efficacy in treatment of chronic infections because previous studies showed that sequences of kDNA minicircle of T. cruzi may integrate in the DNA of the host cell. 29 In this study, PCR amplification products were obtained with nuclear DNA primers PON1/PON2 and template DNA derived from 100% of treated and from 93.7% of untreated Chagas patients, thus showing persistence of the infection, regardless of whether the patient was treated. Since the parasite nuclear DNA does not integrate in the host DNA, the presence of PCR amplification product with T. cruzi nuclear DNA PON1/PON2 was considered evidence of a living infection.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Progressive chronic Chagas heart disease ten years after treatment with anti-Trypanosoma cruzi nitroderivatives.

Lauria-Pires

Braga²,

A³

et al. 2000

Am J Trop Med Hyg

116

View full text Add to dashboard Cite

Abstract. A randomized ten-year follow-up study involving 91 Chagas patients and 41 uninfected controls was undertaken to determine the effectiveness of nitroderivative therapy. Anti-Trypanosoma cruzi antibodies were consistently lower one year after treatment than 10 years thereafter (P Ͻ 0.001). The blood of all treated and 93.7% of untreated Chagas patients yielded polymerase chain reaction (PCR) product from probes annealing to T. cruzi nuclear DNA, indicating active infection. Competitive PCR showed means Ϯ standard deviations of 20.1 Ϯ 22.6 T. cruzi/ml of blood from untreated and 13.8 Ϯ 14.9 from treated Chagas patients, but the differences between means were not statistically significant (P Ͼ 0.05). Electrocardiograms recorded a gamut of alterations several-fold more frequent in Chagas patients, regardless of treatment, than in uninfected controls (P Ͻ 0.001). These results show that nitroderivative therapy for T. cruzi infections is unsatisfactory and cannot be recommended since it fails to eradicate the parasite or change the progression of heart disease in chronic Chagas patients.

show abstract

Section: Discussionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 99%

Progressive chronic Chagas heart disease ten years after treatment with anti-Trypanosoma cruzi nitroderivatives.

Lauria-Pires

Braga²,

A³

et al. 2000

Am J Trop Med Hyg

116

View full text Add to dashboard Cite

show abstract

“…The latter hypothesis has been supported by at least one published paper suggesting possible integration of parasite DNA in the host genome. 31 Another possibility is that T. cruzi organisms present in remote organs may shed their DNA into the blood stream, which is then taken up by the cardiac tissue. 15,30 The central vein of the adrenal gland has been proposed as one potential site of parasite persistence.…”

Section: Discussionmentioning

confidence: 99%

Polymerase chain reaction amplification of three different Trypanosoma cruzi DNA sequences from human chagasic cardiac tissue.

Olivares–Villagómez¹,

McCurley²,

Vnencak‐Jones³

et al. 1998

The American Journal of Tropical Medicine and Hygiene

View full text Add to dashboard Cite

Abstract. Chagas' disease is caused by the hemoflagellate protozoan Trypanosoma cruzi. The most common, serious manifestation of Chagas' disease is a progressive inflammatory cardiomyopathy, which occurs decades after primary infection. The inability to consistently demonstrate T. cruzi by histologic techniques in inflammatory cardiac lesions has suggested that the parasites' persistence may not be required for the pathology of the chronic phase. In this report we further analyze the persistence and localization of T. cruzi DNA in the hearts of seven patients with chronic chagasic cardiomyopathy, along with four indeterminate patients and seven control patients seronegative for T. cruzi infection. In the seven patients with chronic chagasic cardiomyopathy, we extracted DNA from selected inflammatory foci-positive (IFP) and inflammatory foci-negative (IFN) areas of' hematoxylin and eosin-stained cardiac tissue. We then used polymerase chain reaction methodology to amplify three different T. cruzi sequences (a minicircle sequence [MCS], a satellite repetitive sequence [RS], and, a low copy number sequence within the gene coding for a flagellar protein [FPS]). The MCS was detected in ϳ100% of both the IFP and IFN areas analyzed. The RS was detected in 37.5% and 23% of the IFP and IFN areas, respectively (difference not statistically significant; P Ͼ 0.10, degrees of freedom ϭ 1, G test of independence ϭ 1.9522). The FPS was rarely detected (2%), and was only present in DNA extracted from IFP areas. The MCS was also detected in most indeterminate cases (none of whom had inflammatory lesions) although with a markedly diminished amplification signal relative to cardiomyopathy cases. The MCS was not amplified from the cardiac tissues from seronegative controls. These results suggest that the quantity of T. cruzi DNA persisting in hearts of patients with Chagas' disease correlates with cardiomyopathy, but may not be preferentially associated with inflammatory foci.Chagas' disease is caused by the flagellate protozoan Trypanosoma cruzi. Ten to twenty million people in South and Central America are infected with the parasite, and it is estimated that 35 million people are at risk of infection.

show abstract

“…[28][29][30][31] Furthermore, a direct horizontal transfer of sequence of kDNA from T. cruzi to the host cell has been suggested. 32,33 The horizontal transfer of DNA has shed light on features associated with species evolution, by which the position of a taxon in the phylogenesis may be explained. 34,35 The possibility exists that a long process of evolution adapted the flagellates to the intestinal lumen of an insect thus offering a unique opportunity for exchanging genetic material.…”

Section: Discussionmentioning

confidence: 99%

Human IgG1 and IgG4: the main antibodies against Triatoma infestans (Hemiptera: Reduviidae) salivary gland proteins.

Nascimento

Santana²,

Lozzi³

et al. 2001

The American Journal of Tropical Medicine and Hygiene

View full text Add to dashboard Cite

Abstract. The Triatoma infestans salivary gland proteins (TSGP) can induce local and systemic hypersensitivity reactions in humans. IgG antibodies against TSGP were present in higher levels in sera of Chagas disease patients, and in individuals living in triatomine-infested areas than in controls living in triatomine-free areas. TSGP-specific IgG 1 was found in sera of Chagas patients, and of individuals living in triatomine-infested rural areas, and uniquely specific IgG 4 was present in sera of Chagas patients living in triatomine-infested areas, reactive against TSGP. Unique specificities were not detected in sera of individuals reacting against the ubiquitous mosquito Culex quinquifasciatus saliva proteins (CSGP). In conclusion, IgG 1 reactive against TSGP is the main antibody present in individuals living in the triatomine-infested study areas. Also, IgG 4 is found in the sera of insect-transmitted Chagas disease patients living in study areas.

show abstract

Possible integration of Trypanosoma cruzi kDNA minicircles into the host cell genome by infection

Cited by 42 publications

References 34 publications

Progressive chronic Chagas heart disease ten years after treatment with anti-Trypanosoma cruzi nitroderivatives.

Progressive chronic Chagas heart disease ten years after treatment with anti-Trypanosoma cruzi nitroderivatives.

Polymerase chain reaction amplification of three different Trypanosoma cruzi DNA sequences from human chagasic cardiac tissue.

Human IgG1 and IgG4: the main antibodies against Triatoma infestans (Hemiptera: Reduviidae) salivary gland proteins.

Contact Info

Product

Resources

About