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Throughout most of the world, cytomegalovirus (CMV) infection is asymptomatically acquired during childhood. However, in affluent communities, primary infection may be delayed resulting in:

· Infection during pregnancy which may lead to overt or delayed onset of congenital abnormalities in the newborn,

· Infection following blood transfusions which may lead to CMV induced mononucleosis,

· Infection following immunosuppression for organ transplantation which may lead to complications during recovery and/or loss of the organ.

Infection by CMV cannot be clinically diagnosed without confirmation by laboratory testing such as isolation of the virus or the demonstration of a significant rise in specific antibody level.

CMV has the capacity to persist in its human host indefinitely as a latent infection in several glands and the kidneys. Unlike the other herpesviruses, CMV is slow growing, producing a delayed cytopathic effect in cell culture. Cytomegaly is characteristic of a CMV infection resulting in swollen cells containing large paranuclear inclusions.

Prenatal CMV infection may result from transplacental transmission from mother to fetus and is the major infectious cause of mental retardation and other congenital defects in the newborn

In primary CMV infections, the development of antibody is thought to follow the pattern typical of other viral infections, that is, CMV IgM antibody levels rise transiently, while CMV IgG antibody levels rise later but may persist. Recurrence of CMV IgM in reactivated infection is not absolute and appears to be dependent upon the patient population under study (11). Since maternal IgM is not transferred across the placental barrier, the presence of CMV specific IgM present in neonatal serum has a high probability of being an indication for congenital or neonatal infection.

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