Investigation of Epstein-Barr virus or human cytomegalovirus in pediatric gliomas: A retrospective single-center study from Tunisia.
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The involvement of infectious agents in glioma pathogenesis remains controversial. While adult gliomas have been extensively studied, the potential contribution of viral infections to pediatric gliomagenesis is poorly understood. This study aimed to assess the presence of two herpesviruses, Epstein-Barr virus (EBV) and human cytomegalovirus (HCMV), in pediatric gliomas from Tunisian patients. A retrospective investigation of 30 archived pediatric glioma samples was conducted. EBV detection involves PCR targeting the BamM region, in situ hybridization (ISH) for EBER1/2 transcripts, and immunohistochemistry (IHC) for the LMP1 oncoprotein. HCMV was evaluated via PCR amplification of the IE2 gene, ISH of early (E) transcripts, and IHC of IE, E, and late (L) antigens. Clinicopathological features and patient outcomes were also reviewed. The cohort included pilocytic astrocytomas (n = 24), desmoplastic infantile astrocytomas (n = 2), and diffuse pediatric-type high-grade glioma, H3-wild type/IDH-wild type (n = 4). No EBV DNA was detected in any of the tumors. ISH confirmed the absence of EBER expression, and the tumor cells were negative for LMP1. Similarly, no HCMV DNA, RNA transcripts, or IE/E/L antigen expression was identified. This first investigation of EBV and HCMV in pediatric gliomas from Africa and the Arab world provides compelling evidence for these viruses, suggesting that herpesviruses are unlikely to contribute to pediatric gliomagenesis. Larger multicenter studies employing high-sensitivity detection platforms are warranted to definitively rule out viral involvement and explore potential implications for tumor biology and therapy.