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CMV

 human herpesviruses

 Have a cell surface glycoprotein, acts as an Fc rec that can bind the Fc portion of Ig

 replicates in vitro only in human fibroblasts although the virus is often isolated from
epithelial cells of the host.

 replicates very slowly in cultured cells, more slowly than that of HSV or varicella-zoster virus.

PATHOGENESIS

 transmitted person-to-person in several different ways, all requiring close contact with virus-
bearing material.

 There is a 4- to 8-week incubation period in normal older children and adults after viral
exposure

 establishes lifelong latent infections

 can be shed intermittently from the pharynx and in the urine for months to years after
primary infection
 Individuals at greatest risk for CMV disease are those receiving organ transplants, with
malignant tumors, who are receiving chemotherapy, with AIDS.

 Viral excretion is increased and prolonged, and the infection is more apt to become
disseminated.

 Pneumonia is the most common complication.

CONGENITAL AND PERINATAL INFECTION

 Fetal and newborn infections with CMV may be severe

 About 1% of live births annually in the US have congenital CMV

 A high percentage of babies with this disease will exhibit developmental defects and mental
retardation.

TREATMENT AND CONTROL

 Ganciclovir. reduces the incidence of CMV pneumonia also controls progressive hearing loss
in neonates with congenital infections.

 Foscarnet, an analog of inorganic pyrophosphate, is recommended for treatment of


cytomegalovirus retinitis.

 Screening of transplant donors and recipients. The use of blood from seronegative donors
has been recommended when infants will require multiple transfusions.
 Both live and recombinant cytomegalovirus vaccines are under development.

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