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Cytomegalovirus (CMV) is one of the members of the 8 human herpesviruses and is designated as human herpesvirus type 5 (HHV-5). The clinical manifestations of disease due to CMV vary by age and immune status of the host with asymptomatic infection being the most common in children. CMV is a cause of serious disease in newborn infants, immunocompromised solid organ transplant (SOT) and hematopoietic stem cell transplant (HSCT) patients, and HIV-infected individuals. The virus also is a cause of infectious mononucleosis. Hence, CMV is a pathogen of great importance in all aspects of pediatric medicine.


Taxonomically, CMV is referred to as a betaherpesvirus, based on its propensity to infect mononuclear cells and lymphocytes and on its molecular phylogenetic relationship to human herpesvirus type 6 (HHV-6) and human herpesvirus type 7 (HHV-7). The virus consists of a double-stranded DNA genome of approximately 235 kbp. As with the other herpesviruses, the structure of the viral particle is that of an icosahedral DNA-containing capsid, surrounded by a lipid bilayer outer envelope that contains the virally encoded glycoproteins, which are the major targets of host neutralizing antibody responses. The proteinaceous layer between the envelope and the inner capsid, the viral tegument, contains proteins that are targets of host cell–mediated immune responses.

Little is known about the molecular mechanisms responsible for the pathogenesis of tissue damage caused by CMV, particularly for congenital CMV infection. Because CMV can infect endothelial cells, it has been postulated that a viral angiitis may be responsible for perfusion failure of developing brain with resultant maldevelopment. Others have postulated a direct teratogenic effect of CMV on the developing fetus. Observation of CMV-induced alternations in the cell cycle and damage to chromosomes supports this speculation, although this hypothesis has been difficult to experimentally verify. Infection of the fetal brain, particularly during the first trimester, induces several perturbations in neural development, including neuronal migration defects. This can lead to the characteristic brain pathologies associated with severe fetal infection.

Immunity to CMV is complex and involves both humoral and cell-mediated responses. Envelope glycoproteins and tegument phosphoproteins are important in humoral and cellular immunity, respectively. More recent investigations into the molecular biology of CMV have revealed the presence of many genes that modulate the host immune responses. These include genes that inhibit major histocompatibility complex (MHC) class I antigen presentation, homologs of cellular G-protein–coupled receptors, a homolog of the cellular major histocompatibility class I gene, homologs of chemokines, and a homolog of the tumor necrosis factor receptor superfamily. These genes may contribute to the ability of CMV to escape immune clearance, which in turn allows for reinfection of seropositive individuals with new CMV strains with different antigenic specificities. CMV immune evasion is an important factor in congenital infection (because of reinfection in seropositive women followed by vertical transmission during pregnancy) and complicates the development of vaccines.


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