The virus is transmitted orally through saliva droplets infecting both B lymphocytes and epithelial cells of the oronasopharynx. anti-EpsteinCBarr Computer virus serology in gastric cancer and precursor lesions following PRISMA guidelines. Patients were classified according to the Correa cascade of gastric lesions and whether they were positive or unfavorable by EBER-hybridization (EpsteinCBarr Virus-associated gastric cancer and EpsteinCBarr Virus-nonassociated gastric cancer, respectively). Results: We retrieved 16 articles involving 9735 subjects from 12 different countries and 4 databases, PubMed, SciELO, Scopus, and Google Scholar. Higher antibody titers were observed not only in EpsteinCBarr Virus-associated gastric cancer than in EpsteinCBarr Virus-nonassociated gastric cancer but also in EpsteinCBarr Virus-nonassociated gastric cancer LG-100064 and gastric cancerCprecursor lesions when compared with patients with moderate dyspepsia or healthy controls. In all cases, the associations were predominantly with antibodies directed against lytic cycle antigens. Conclusion: Data support the role of LG-100064 EpsteinCBarr Computer virus lytic reactivation in the development of advanced gastric lesions. However, more studies are needed to LG-100064 confirm these associations, particularly the association with lesions considered unfavorable by EBER-hybridization, and to establish a set of antibodies and thresholds indicative of enhanced risk to develop these lesions. Keywords: EBV, antibodies, serology, gastric cancer, EBVaGC, gastric cancer risk Introduction Gastric cancer (GC) is the fourth deadliest cancer worldwide. 1 It has a well-recognized infectious etiology 2 with contamination is considered the main cause of mucosal inflammation that drives the neoplastic pathway. 5 Over the last century, the declining prevalence of contamination in many parts of the world has resulted in a declining incidence of GC. According to the Lauren classification, there are 2 major histologies of GC: the intestinal- and diffuse-types. These 2 types have different natural histories, the former evolving as progressive inflammatory lesions starting with a nonatrophic gastritis (NAG), which becomes atrophic gastritis (AG), intestinal metaplasia (IM), dysplasia (DYS), and cancer (a sequence known as Correa’s cascade), 6 while for the latter there are not known intermediate pre-cancerous lesions, although it still originates from an inflammatory NAG. Gastric cancer clinical course varies with stage at diagnosis. In the United States, malignancy diagnosed before spreading outside the stomach has a 5-12 months survival rate of 70.3%. On the other hand, when it has already LG-100064 spread to surrounding tissues and/or regional lymph nodes, or to distant parts of the body, the 5-12 months survival decreases to 32% and 5.8%, respectively. 7 Unfortunately, most patients are diagnosed at advanced stages of the disease in both developed and developing nations. Early detection screening and eradication programs have been implemented in South-East Asian countries with a high incidence of GC to reduce its mortality. 8 EpsteinCBarr Computer virus is usually a lymphotropic herpesvirus that infects about 95% of the world’s populace. The computer virus is usually transmitted orally through saliva droplets infecting both B lymphocytes and epithelial cells of the oronasopharynx. Primary contamination usually happens during childhood and persists for the lifetime of the infected individual, with memory B cells being the site of lifelong persistence. 9 Contamination of the epithelial cells increases the amount of viral particles released into saliva facilitating transmission to new hosts.10,11 It is not clear how EBV infects gastric epithelial cells and in which step of the Correas cascade EBV is already present in the progressing gastric lesion. EpsteinCBarr Computer virus exhibits a bipartite life cycle alternating between latent and lytic phases. During latent contamination, most of the viral genome is usually epigenetically silenced, leaving the expression of only a Palmitoyl Pentapeptide handful of genes. Suppression of viral gene expression facilitates persistence since the computer virus can hide from antagonistic host immune responses. Latency is the favored viral program upon contamination of B lymphocytes, and it is the program found in EBV-associated neoplasms as several of the latent genes exhibit oncogenic activity. 12 Latent expression is limited to the EBV nuclear antigens (EBNA1, EBNA2, EBNA3A, 3B and 3C, and EBNA-LP (leader protein)) and the latent membrane.
