HUMAN CYTOMEGALOVIRUS (HCMV) LEUKODNAEMIA CORRELATES MORE CLOSELY WITH CLINICAL SYMPTOMS THAN ANTIGENEMIA AND VIREMIA IN HEART AND HEART-LUNG TRANSPLANT RECIPIENTS WITH PRIMARY HCMV INFECTION

Background, In the last few years, human cytomegalovirus (HCMV) viremi a, pp65 antigenemia, and leuko- and plasma-DNAemia have been developed to quantitate virus in blood of immunocompromised patients with HCMV infection. However thus far, no conclusive studies have been performed to define the correlation of each of the different assays With clinic al symptoms in primary HCMV infections. Methods. This correlation was investigated in a population of 20 heart and heart-lung transplant rec ipients with primary HCMV infection using standardized virological met hods. Results. Median peak HCMV viremia, antigenemia, and leukoDNAemia levels were 110 (0-2,000) p72-positive fibroblasts, 450 (27-2,000) pp 65-positive leukocytes, and >10,000 (1,358-10,000) genome equivalents (GE) in the 14 symptomatic patients and 18 (1-130) p72-positive fibrob lasts, 86.5 (5-350) pp65-positive leukocytes, and 248 (10-863) GE in t he six asymptomatic patients, respectively. The difference was statist ically significant for antigenemia (P=0.009) and leukoDNAemia (P<0.000 1). However, on an individual basis, unlike viremia and antigenemia, a ll DNA peaks of the 6 asymptomatic patients were below the DNA range o f the 14 symptomatic patients (<1,000 GE), while all the 14 symptomati c patients had DNA peaks higher than those of asymptomatic patients (> 1,000 GE). Follow-up confirmed these results, showing that 1,000-2,000 GE was the threshold zone for emergence of clinical symptoms. Symptom s were never observed in patients with secondary DNA peaks, except for one patient suffering from an HCMV organ localization (HCMV gastritis ), Conclusions. LeukoDNAemia is the viral parameter of choice for moni toring of primary HCMV infections and antiviral treatment in heart and heart-lung transplant recipients. In this patient population, antigen -emia-guided preemptive therapy could be replaced by leukoDNAemia-base d antiviral therapy.