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EBV is particularly lymphotropic regarding its latency, meaning that it preferentially targets lymphocytes as its immunological niche. During the establishment of the complex virus\u2013host relationships, the virus influences the human host cell transcriptome inducing changes in RNA quantity and quality aided by a multitude of virally encoded molecules such as microRNAs, lncRNAs, peptides, and proteins. Quantitative changes in human gene expression of infected host cells are due to epigenetic mechanisms, such as altered promoter methylation patterns and altered microRNA\u2010 or lncRNA\u2010based post\u2010transcriptional gene regulation mechanisms. The quality of the human transcriptome is altered including changes in chemical RNA modifications and alterations in alternative splicing (AS) patterns. These molecular mechanisms contribute to the immune evasion of EBV, enhanced host cell proliferation and desensitization to apoptosis induction. These mechanisms are highly relevant to the process of malignant transformation of infected host cells, highlighting the tumorigenic potential of EBV. This review article addresses the role of AS in malignant transformation of EBV\u2010infected host cells. For this purpose, publicly available transcriptome datasets from EBV\u2010positive human Burkitt lymphomas (BL) were analyzed in an EBV\u2010copy number dependent manner. 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