Aetiology
Cytomegalovirus (CMV) is a member of the herpes virus family.[3] It contains a genome of double-stranded linear DNA, an icosahedral viral capsid, and a viral envelope protein that includes the highly immunogenic glycoprotein B. The biological characteristic of all herpes viruses, including CMV, is the ability to establish latency after primary infection. Such a biological characteristic allows for periodic viral re-activations during the life of the human host.[3]
Routes of transmission include person-to-person spread (kissing, intimate contact, sexual intercourse), vertical transmission (mother-to-child transmission resulting in congenital infection), blood transfusion, and organ or haematopoietic stem cell transplantation.
Pathophysiology
CMV infects a variety of cells, including mononuclear leukocytes and endothelial cells. It has a replication cycle of approximately 1 day in CMV-naive individuals, resulting in a viral progeny.
During infection, CMV antigens trigger the innate immune system to secrete various antiviral peptides, including interferon. Some studies suggest that this is partly mediated by a toll-like receptor family of pattern recognition molecules.[15][16] Subsequently, the innate immune response orchestrates the development of humoral and cell-mediated adaptive immunity, which eventually controls the viral infection, thereby leading to a state of latency.[17] Factors that impair innate and adaptive immune responses predispose to uncontrolled viral reactivation and replication, which lead to viral cytopathic effects and clinical illness.
Classification
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