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Cytomegalovirus (CMV) Antibodies, IgG
Test CodeCMVG
Alias/See Also
Epic: LAB467
Preferred Specimen
Specimen Type: Serum
Collection Container: Serum gel
Specimen Volume: 3 mL
Minimum Volume
0.5 mL
Instructions
Centrifuge and separate cells after clot formation and within 4 hours of collection
Transport Container
Plastic vial
Specimen Stability
Room temperature: Undefined
Refrigerated: 48 hours
Frozen: >2 days
Reject Criteria (Eg, hemolysis? Lipemia? Thaw/Other?)
Unlabeled, mislabeled, wrong tube type, QNS, severely hemolyzed samples (hemolysis index >1000) and any sample from which the lipid layer has not been removed.(triglyceride >3000 mg/dL). Use ultracentrifuge to remove lipid layer.
Methodology
Chemiluminescent Immunoassay (CLIA)
Setup Schedule
Daily
Report Available
1 day
Reference Range
Negative
Clinical Significance
Human cytomegalovirus (hCMV) is a herpes virus. It is ubiquitous, species-specific, and spread by close human contact .
Primary infection may be acquired through different transmission routes and in different periods of life (e.g., congenital, perinatal and post-natal infections). Following primary infection, hCMV enters a latency phase during which the virus can be found in B lymphocytes. Subsequent reactivation of viral replication (secondary infection) may take place concomitantly with changes in the relationship between host and virus. Reinfection with exogenous virus can occur in subjects with deficiency of cellular immunity even when antibodies to hCMV are already present .
hCMV infection may be transmitted transplacentally (congenital) or at birth (perinatal). If seronegative women contract primary hCMV infection during pregnancy, the infection is transmitted to the fetus in about 40% of the cases and sequelae may be spontaneous abortion, stillbirth or neonatal malformation. The clinical picture of congenital hCMV infection may be mild to severe and includes psychomotor retardation, deafness, retinochoroiditis, microcephaly, hydrocephalus, cardiac disease, hepatitis, hepatosplenomegaly, or thrombocytopoenia .
Most individuals (40-90%) acquire primary hCMV infection during childhood or adulthood. Post-natal infections are transmitted through close contact with infected biological fluids (urine, saliva, breast milk, semen, cervical secretions, feces), infected blood products, and, occasionally, organ transplants. In immunocompetent individuals, the clinical picture of post-natal hCMV infection is usually mild or asymptomatic. The most common signs include fever, malaise, and increased serum transaminase levels without jaundice .
By contrast in immunocompromised patients (organ transplant recipients, patients with AIDS, lymphoproliferative diseases, or cancer), symptoms may be severe because of disseminated and/or visceral infection, and may include splenomegaly, pneumonia, hemolytic anemia, myocarditis and encephalitis. In these patients the disease may be fatal .
The immune response to hCMV involves synthesis of IgM antibodies some weeks after infection by hCMV, and later, IgG antibodies. Levels of IgM to hCMV usually increase for some weeks and decrease slowly thereafter, in four to six months. Occasionally, IgM may circulate for years. IgG antibodies rise gradually and persist for the rest of the host life.
The specific IgG assay is useful in distinguishing subjects who have been exposed to the virus from those who have not.
Primary infection may be acquired through different transmission routes and in different periods of life (e.g., congenital, perinatal and post-natal infections). Following primary infection, hCMV enters a latency phase during which the virus can be found in B lymphocytes. Subsequent reactivation of viral replication (secondary infection) may take place concomitantly with changes in the relationship between host and virus. Reinfection with exogenous virus can occur in subjects with deficiency of cellular immunity even when antibodies to hCMV are already present .
hCMV infection may be transmitted transplacentally (congenital) or at birth (perinatal). If seronegative women contract primary hCMV infection during pregnancy, the infection is transmitted to the fetus in about 40% of the cases and sequelae may be spontaneous abortion, stillbirth or neonatal malformation. The clinical picture of congenital hCMV infection may be mild to severe and includes psychomotor retardation, deafness, retinochoroiditis, microcephaly, hydrocephalus, cardiac disease, hepatitis, hepatosplenomegaly, or thrombocytopoenia .
Most individuals (40-90%) acquire primary hCMV infection during childhood or adulthood. Post-natal infections are transmitted through close contact with infected biological fluids (urine, saliva, breast milk, semen, cervical secretions, feces), infected blood products, and, occasionally, organ transplants. In immunocompetent individuals, the clinical picture of post-natal hCMV infection is usually mild or asymptomatic. The most common signs include fever, malaise, and increased serum transaminase levels without jaundice .
By contrast in immunocompromised patients (organ transplant recipients, patients with AIDS, lymphoproliferative diseases, or cancer), symptoms may be severe because of disseminated and/or visceral infection, and may include splenomegaly, pneumonia, hemolytic anemia, myocarditis and encephalitis. In these patients the disease may be fatal .
The immune response to hCMV involves synthesis of IgM antibodies some weeks after infection by hCMV, and later, IgG antibodies. Levels of IgM to hCMV usually increase for some weeks and decrease slowly thereafter, in four to six months. Occasionally, IgM may circulate for years. IgG antibodies rise gradually and persist for the rest of the host life.
The specific IgG assay is useful in distinguishing subjects who have been exposed to the virus from those who have not.
Performing Laboratory
Inova Laboratories
2832 Juniper Street
Fairfax, VA 22031
Last Updated: March 6, 2023
Last Review: N. Wolford, March 6, 2023