During the interaction between a virus and its host, a complex interplay arises between the host's defence mechanisms and the viral survival strategies. This interaction impacts not only viral replication and the viral lifecycle but also affects the host's homeostasis, including cellular genetics and immune responses. The outcomes of host-virus interactions can vary widely, ranging from successful pathogen clearance to severe disease or even death, influenced by factors such as host genetics, age, comorbidities, and environmental conditions. Viruses adeptly manipulate cellular machinery and metabolism, reprogram signalling pathways, and undermine immune responses to enhance their survival. A key strategy employed by viruses is immune evasion, utilising various techniques to bypass the host's immunovigilance. These strategies not only encourage persistent infections but also raise concerns about oncogenic potential, particularly in hematologic malignancies like acute lymphoblastic leukaemia (ALL). Such mechanisms may play a pivotal role in the alterations induced by viral contributions that disrupt immune surveillance and foster malignancy. This review seeks to elucidate the potential role of human cytomegalovirus (HCMV) as a risk factor and etiological contributor to the development of ALL in children. Although HCMV has not been officially recognized as an oncogenic virus, emerging evidence suggests that early-life infection may predispose to malignant transformation by promoting oncogenic pathways and immune dysregulation.
Ruvalcaba-Hernández et al. (Thu,) studied this question.
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