scholarly journals Detection of Epstein-Barr Virus DNA in Gastric Biopsies of Pediatric Patients with Dyspepsia

Pathogens ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 623 ◽  
Author(s):  
Abigail Morales-Sánchez ◽  
Javier Torres ◽  
María G. Cardenas-Mondragón ◽  
Carolina Romo-González ◽  
Margarita Camorlinga-Ponce ◽  
...  

In this study, we assessed the presence of Epstein-Barr virus (EBV) in gastric samples derived from pediatric patients with dyspeptic symptoms, aiming to understand whether EBV participates in the development of early gastric lesions influencing chronic inflammation, in conjunction with the Helicobacter pylori (Hp) bacterium. We analyzed EBV load in 236 gastric biopsies derived from 186 pediatric patients with chronic dyspepsia and compared it with EBV serology, Hp load and serology, and with immune cell infiltration. We found that 7.5% of patients were positive for EBV load, ranging from 240 to 29,685 genomic copies/μg of DNA. Hp genomic sequences were found in 24.7% of patients. EBV positive samples did not correlate with Hp status and were characterized by absent to moderate immune cell infiltration. To our knowledge, this is the first study addressing EBV load in the stomach in a large cohort of pediatric patients with dyspeptic symptoms, providing evidence of EBV localization in the gastric mucosa in early inflammatory lesions. The lack of correlation between EBV and both Hp infection and inflammation is perhaps explained by independent pathogenic mechanisms or because of the randomness of the gastritis sampling. This is also supported by a moderate association between EBV load and serology.

2021 ◽  
Author(s):  
Jing Lin ◽  
Miaofang Su ◽  
Jiaolong Zheng ◽  
Haicong Wu ◽  
Lei Gu ◽  
...  

Abstract Background: Chronic active Epstein-Barr virus hepatitis (CAEBVH) in adult patients is a rare and highly lethal disease characterized by hepatitis and hepatomegaly.Aims: To investigate the clinicopathological features and pathogenic mechanisms in patients with CAEBVH.Methods:10 adult patients confirmed CAEBVH infection were collected. The clinicopathological characteristics were summarized and analyzed by clinical data. Flow cytometry to detect peripheral blood immune cell phenotypes, second-generation sequencing methods to explore pathogenic mechanisms, and immunohistochemical methods to verify pathogenic mechanisms.Results: The clinical features included splenomegaly, hepatomegaly, abnormal liver function, and CD8+T lymphopenia. HE also showed lymphocytic infiltration in liver tissue. EBER-ISH in lymphocytes of liver tissues were positive. Whole exon sequencing showed mutant genes were primarily enriched in 'T cell activation' and 'Complement and coagulation cascades'. The expression of CD8 in the CAEBVH group was higher than the controls in liver tissue (p<0.05). The same as the expression of Fas, FasL, Caspase-8, and TUNEL assay (p<0.05). Complement 1q (C1q) of liver sinusoidal endothelial cells (LSECs) and Glisson's capsule (GC), as well as Complement 3d (C3d) of LSECs, were a higher expression in CAEBV infection than controls (p<0.05).Conclusion: Fas/FasL and complement activation were involved in adult patients with chronic active Epstein-Barr virus hepatitis.


2012 ◽  
Vol 84 (10) ◽  
pp. 1697-1697
Author(s):  
Mario Alejandro Lorenzetti ◽  
Marina Inés Gutiérrez ◽  
Jaime Altcheh ◽  
Guillermo Moscatelli ◽  
Samanta Moroni ◽  
...  

2001 ◽  
Vol 124 (2) ◽  
pp. 188-194
Author(s):  
Tommy Shpitzer ◽  
Jeroen D. F. Kerrebijn ◽  
Jeremy L. Freeman ◽  
Warren Hartwick ◽  
Yuriko Saiki ◽  
...  

Author(s):  
Katarzyna Bąbol-Pokora ◽  
Magdalena Wołowiec ◽  
Katarzyna Popko ◽  
Aleksandra Jaworowska ◽  
Yenan T. Bryceson ◽  
...  

AbstractHemophagocytic lymphohistiocytosis (HLH) is a clinical syndrome of life-threatening inflammation caused by an excessive, prolonged and ineffective immune response. An increasing number of HLH cases is recognized in Poland, but the genetic causes of familial HLH (FHL) have not been reported. We investigated the molecular genetics and associated outcomes of pediatric patients who met HLH criteria. We studied 54 patients with HLH, 36 of whom received genetic studies. Twenty-five patients were subjected to direct sequencing of the PRF1, UNC13D, STX11, XIAP and SH2D1A genes. Additionally, 11 patients were subjected to targeted next-generation sequencing. In our study group, 17 patients (31%) were diagnosed with primary HLH, with bi-allelic FHL variants identified in 13 (36%) patients whereas hemizygous changes were identified in 4 patients with X-linked lymphoproliferative diseases. In addition, one patient was diagnosed with X-linked immunodeficiency with magnesium defect, Epstein–Barr virus infection and neoplasia due to a hemizygous MAGT1 variant; another newborn was diagnosed with auto-inflammatory syndrome caused by MVK variants. The majority (65%) of FHL patients carried UNC13D pathogenic variants, whereas PRF1 variants occurred in two patients. Novel variants in UNC13D, PRF1 and XIAP were detected. Epstein–Barr virus was the most common trigger noted in 23 (65%) of the patients with secondary HLH. In three patients with secondary HLH, heterozygous variants of FHL genes were found. Overall survival for the entire study group was 74% with a median of 3.6 years of follow-up. Our results highlight the diversity of molecular causes of primary HLH in Poland.


2013 ◽  
Vol 32 (3) ◽  
pp. 184-191 ◽  
Author(s):  
Nancy Elawabdeh ◽  
Brent M. Cone ◽  
Carlos R. Abramowsky ◽  
David M. Wrubel ◽  
Hans Grossniklaus ◽  
...  

2009 ◽  
Vol 81 (11) ◽  
pp. 1912-1917 ◽  
Author(s):  
Mario Alejandro Lorenzetti ◽  
Marina Inés Gutiérrez ◽  
Jaime Altcheh ◽  
Guillermo Moscatelli ◽  
Samanta Moroni ◽  
...  

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