The clinical presentation of CMV infection is highly inﬂuenced by the immune ﬁtness of the host ( 14). Its reactivation in healthy immunocompetent hosts, which occurs intermittently throughout life, triggers immuno- logic memory that leads to effective control of viral rep- lication ( 15). On the other hand, the loss of CMV-speciﬁc CD4+ and CD8+ T-cells in the immunocompromised host, such as those with human immunodeﬁciency virus (HIV) infection, recipients of solid-organ transplant (SOT), or hematopoietic stem-cell transplant (HSCT), may permit uncontrolled viral replication, leading sub- sequently to clinical disease ( 16, 17)(Table 1).
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