CMV Viral Load

Useful For

Assessing viral response to antiviral treatment as measured by changes in CMV DNA levels. This test is not intended as a diagnostic test to confirm the presence of CMV infection (see CMV virus culture).


Method Name

Quantitative PCR


Reporting Name

CMV viral load





Cytomegalo Inclusion Disease (CMID)

Human Herpes Virus 5


Specimen Required



Specimen Minimum Volume

Plasma: 1.2 mL


Transport Temperature

Specimen Room temperature Refrigerated Frozen
Whole Blood* NO NO NO
Plasma NO YES** YES***

* Separate plasma from whole blood within 6 hours of collection by centrifugation at 800-1600 x g for 20 mins.

**The samples should be stored for not more than 7 days at 2-8°C.

***For longer delay, freeze at -20°C or below and transport on dry ice.


Reject Due To

Specimens other than Plasma
Anticoagulants other than EDTA REJECT
Hemolysis OK
Lipemia OK
Icteric OK

Useful For

The test is intended for use in conjunction with clinical presentation and other laboratory markers as an aid in assessing viral response to antiviral treatment as measured by changes in CMV DNA levels. This assay is NOT intended to be used as a screening test for blood or blood products for the presence of CMV or as a diagnostic test to confirm the presence if CMV infection.


Clinical Information

Cytomegalovirus (CMV) is a significant cause of morbidity and mortality, especially in organ transplant recipients and immunocompromised individuals. In transplant recipients CMV infection/disease has been associated with acute rejection (renal transplant), and chronic graft dysfunction (including cardiac transplant vasculopathy and bronchiolitis oblitirans syndrome in lung transplantation). CMV is associated with with cirrhosis and graft failure after liver transplantation and with more aggressive relapse of hepatitis C with fibrosis. CMV is immunosuppressive, increasing the risk of opportunistic superinfections, particularly those due to fungi. CMV may also work synergistically with other agents to cause disease (EBV and post-transplant lymphoproliferative disorders, viral syndromes and graft loss with human herpes virus 6 and HHV 7).

Peripheral blood mononuclear cells and endothelial cells appear to be the major sites of infection. CMV remains in a latent stage in monocytes/macrophages in humans. Latently infected individuals may shed the virus in their body fluids and thus infect others. Neonates, immunocompromised individuals, transplant patients and AIDS patients are usually at higher risk for developing severe CMV infections that lead to a higher rate of morbidity and mortality. Severe clinical manifestations of CMV disease include retinitis, gastroenteritis, hepatitis, encephalitis, esophagitis, enterocolitis, pancreatitis and pneumonia.


Laboratory methods for the diagnosis of disseminated infection and active visceral disease for human Cytomegalovirus include isolation of virus by culture from peripheral blood leukocytes (PBL), serological methods etc. Direct detection of CMV DNA in plasma using PCR has shown to correlate well with PBL culture positivity and with increased risk for developing systemic CMV disease. CMV disease is clearly defined by high viral load, which points to an important role of viral load in disease pathogenesis. Quantitative assessments of CMV DNA levels have shown that high viral loads, as well as increases of viral load over time, have the worst prognoses. Quantitative PCR also allow for monitoring of antiviral treatment efficacy, and indirect evaluation of viral resistance.


Viral loads can be used as a surrogate marker for risk. Trends are more useful than individual assay results as the rate of rise of viral load as well as initial quantitative viral load assessment are independent indicators of CMV disease risk. Interpretation of CMV viral load kinetics is best considered with the guidance of transplant specialist and infectious disease specialists.


CMV disease, particularly in the gastrointestinal tract and the lungs can occur in the absence of detectable viral load in peripheral blood.



Reference Values

NOT DETECTED (<150 copies/mL)



CMV DNA DETECTED: quantitative value reported as copies/mL


Clinical Reference

Crumpacker II, C. S., and Zhang, J. L. 2010. Cytomegalovirus, p. 1971-1987. In Mandell, D., Bennett, J. E., and Dolin, R. Principles and practice of infectious diseases, 7th ed., vol. 2. Churchill Livingstone, Elsevier, Philadelphia, PA.


Hodinka, R. L. 2007. Human Cytomegalovirus, p. 1549-1563. In Murray, P. R., Baron, E. J., Jorgensen, J. H., Landry, M. L., and Pfaller, M. A. Manual of Clinical Microbiology, 9th ed., vol. 2. ASM Press, American Society for Microbiology, Washington, DC.


Preiksaitis, JK., Brennan DC., Fishman J, and Allen U. 2005. Canadian Society of Transplantation Consensus Workshop on Cytomegalovirus Management in Solid Organ Transplantation Final Report. Am J Transplant. 5:218-227.

CMV viral load

Status Days Analytic Time Maximum Laboratory Time Specimen Retention
Routine Thursday 7h 6 days 2 years



Method Description

The COBAS® AmpliPrep/COBAS® TaqMan® CMV test is based on nucleic extraction from plasma, PCR amplification of target DNA using CMV specific primers, detection of amplified product by oligonucleotide probes specific for the target(s). Quantitative determination of amplified product is accomplished by comparing the amplified product signal to that of a quantitation standard for each specimen.


Performing Laboratory Location

Newfoundland & Labrador Public Health Laboratory

St. John’s


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