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and M.G.C.-M.; performed the Hp and EBV serology, respectively. of the randomness of the gastritis sampling. This is also supported by a moderate association between EBV load and serology. (Hp) infection, a stomach resident bacterium with BMS-265246 a plethora of mechanisms to counteract the acidic pH and colonize the gastric mucosa. About 10% of GC are associated with Epstein-Barr virus (EBV) infection, a persistent pathogen most often acquired in early childhood. EBV is considered BMS-265246 a lymphotropic virus because it mainly infects and persists in B lymphocytes. Yet, EBV is also able to infect epithelial cells, which facilitates viral transmission to new hosts [2]. For this, EBV colonizes the Waldeyers ring lymph nodes in the oropharynx, where epithelial cells and lymphoid tissue intimately coexist [2]. How and when EBV reaches the gastric mucosa remains unclear, as well as whether it may contribute with dyspeptic symptoms in early gastric lesions. We have previously reported that elevated levels of antibodies directed against EBV lytic proteins significantly correlate with advanced gastric lesions and with enhanced stomach infiltration of polymorphonuclear (PMN) and mononuclear (MN) immune cells, supporting the idea that EBV reactivation in the stomach is also contributing to the chronic inflammatory process, in conjunction with Hp [3,4,5]. Indeed, we observed that even children younger than ten years old with highly inflammatory and symptomatic gastritis already had elevated levels of anti-EBV antibodies [3]. In this study, we aimed to find evidence of viral loads already present in the gastric mucosa of children with dyspepsia, and address whether or not load correlated with gastric inflammation markers and Hp status. 2. Materials and Methods 2.1. Patients and Clinical Samples This study was approved by the Ethical, Biosafety, and Scientific Institutional Review Boards of the Childrens Hospital of Mexico Federico Gmez and the Pediatrics Hospital of the Mexican Social Security Institute. The study was performed on frozen archived samples, parents or guardians of the enrolled patients agreed to sign a letter of consent. All patients attended the gastroenterology unit due to dyspeptic symptoms characterized by chronic abdominal pain present for BMS-265246 at least six months. Clinical diagnosis as nonatrophic gastritis was based on endoscopy, histology, and clinical presentation. Patients under treatment with antiacid, antibiotics or proton pump inhibitors during the three weeks prior to sample collection were excluded. Blood and gastric tissue samples were collected at the time of diagnosis. The study started with 356 frozen samples corresponding to 257 patients. Paired samples of the stomach antrum and corpus were collected from some of the patients. One biopsy sample was used for DNA extraction and estimation of viral and bacterial loads BMS-265246 by PCR-based approaches. The extracted DNA was first tested for quality using a qPCR directed against the endogenous -actin gene, only samples with good DNA quality were chosen to continue BMS-265246 in the study. Overall, the samples we included in the study were the following236 gastric tissue samples derived from 186 patients; only antrum tissues from 86 patients, only corpus tissues from 50 patients, and paired antrum and corpus tissues from 50 patients, for a total of 136 samples from antrum and 100 samples from corpus. Of the 186 patients, we had information of EBV and Hp serology for 134 (73%) of them. Serology Mouse monoclonal to OTX2 and viral load results were.