Frequency of Epstein-Barr virus DNA sequences in human gliomas

Abstract

CONTEXT AND OBJECTIVE: The Epstein-Barr virus (EBV) is the most common cause of infectious mononucleosis and is also associated with several human tumors, including Burkitt's lymphoma, Hodgkin's lymphoma, some cases of gastric carcinoma and nasopharyngeal carcinoma, among other neoplasms. The aim of this study was to screen 75 primary gliomas for the presence of specific EBV DNA sequences by means of the polymerase chain reaction (PCR), with confirmation by direct sequencing. DESIGN AND SETTING: Prevalence study on EBV molecular genetics at a molecular pathology laboratory in a university hospital and at an applied genetics laboratory in a national institution. METHODS: A total of 75 primary glioma biopsies and 6 others from other tumors from the central nervous system were obtained. The tissues were immediately frozen for subsequent DNA extraction by means of traditional methods using proteinase K digestion and extraction with a phenol-chloroform-isoamyl alcohol mixture. DNA was precipitated with ethanol, resuspended in buffer and stored. The PCRs were carried out using primers for amplification of the EBV BamM region. Positive and negative controls were added to each reaction. The PCR products were used for direct sequencing for confirmation. RESULTS:The viral sequences were positive in 11/75 (14.7%) of our samples. CONCLUSION: The prevalence of EBV DNA was 11/75 (14.7%) in our glioma collection. Further molecular and epidemiological studies are needed to establish the possible role played by EBV in the tumorigenesis of gliomas. RESUMO

Epstein–Barr Virus in Gliomas: Cause, Association, or Artifact?

“…These results are in contrast to the study from Slovenia where only high-grade gliomas were positive for EBV ( 34 ). In addition, Fonesca et al ( 79 ) also found EBV in one oligoastrocytoma and one ependymoma, but none at all in other CNS tumors including two non-HL—a tumor type in which EBV association has been reported previously ( 75 ). The amplified EBV gene sequences obtained from gliomas were well matched with published EBV genome sequences with an identicalness rate of 95.5% implying that EBV virus was indeed present in these samples.…”

“…A study by Fonesca et al ( 79 ) aimed to screen 75 primary glioma biopsy specimens from a cancer centre in Rio de Janeiro, Brazil, for the presence of EBV using PCR with confirmation using direct sequencing. To detect EBV in tumor samples, a 288 bp fragment of EBV bam region was amplified and later sequenced to confirm viral DNA in GeneBank data sets.…”

Prevalence of Neurotropic Viruses in Malignant Glioma and Their Onco-Modulatory Potential

“…In a similar manner, tumours overcome immune surveillance during their malignant progression, as has also been demonstrated in the case of EBV infection, which is present in about 90% of the world population. EBV has been associated with selected human tumours, including Burkitt's lymphoma and Hodgkin's lymphoma, and less frequently in vivo 31: 221-230 (2017) 226 for some cases of gastric carcinoma and nasopharyngeal carcinoma, depending on the geographic and ethnic distribution of the populations (10,29). In glioma, EBV was detected in about 30% of samples (9/35) obtained from patients with pilocytic astrocytoma (45).…”

“…In glioma, EBV was detected in about 30% of samples (9/35) obtained from patients with pilocytic astrocytoma (45). Recently, Fonseca et al studied 75 fresh frozen glioma tissues of different histological subtypes using conventional PCR, and they reported 14.7% prevalence of EBV DNA in WHO III (2/11) and WHO IV (1/11) gliomas (29). Similarly, in the present study, we found EBV DNA in three out of 45 tissues, but not in the corresponding sera, possibly due to the very low amounts of EBV.…”

“…A metaanalysis of 16 reports by Salomon et al (25) confirmed the concept that there is no clear-cut evidence for a role of HCMV in GBM tumorigenesis. Similarly, specific roles of other herpes viruses in glioma initiation have not been demonstrated to date (11,(26)(27)(28)(29)(30).…”