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Cytomegalovirus, a member of herpesviridae family, is a double-stranded DNA virus [1, 2] which can be a leading cause of viral-associated congenital infections [3] or either can be acquired [1]. Between 50 to 80 percent of the world’s population is seropositive for CMV [4]. Most clinical disease occurs in individuals previously infected with CMV (seropositive) and therefore represents either re-activation of latent infection or re-infection (de novo) with a novel strain [5]. In immunocompetent host, it is typically asymptomatic or is responsible for mild undifferentiated viral symptoms and mononucleosislike syndrome [4]. Rarely, serious CMV infection has occurred in individuals with healthy immune system [6]. In contrast to immuno-competent patients, immuno-compromised patients may experience systemic and end-organ disease primarily due to virus reactivation as a result of impaired immune system consistency. Systemic CMV disease is characterized by fever, pancytopenia, and inflammatory changes in multiple organs [4].

CMV infection is controlled by virus-specific CD4+ and CD8+ cytotoxic T-lymphocytes [7]. Previously, it was demonstrated that conditions like HIV infection, hematopoietic stem cell transplantation (HSCT), solid organ transplantation [8], and some immunosuppressive agents like ibrutinib [9], dasatinib [4], alemtuzumab [10], steroids, fludarabin, and high-dose cyclophosphamide [11] can impair T-cell mediated immunity but standard chemotherapy alone for pediatric leukemia mainly depletes humoral rather than cellular immunity [12]. Therefore, CMV disease development is rare in pediatric non-HSCT ALL being on chemotherapy …