Cytomegalovirus (CMV) DNA load was analyzed as a marker for relapse of CMV infection in 24 solid organ transplant patients with CMV infection or disease who received a fixed 14-day course of intravenous ganciclovir. Viral load was measured in blood samples obtained before and at the completion of treatment. Eight (33%) of 24 patients developed relapsing CMV infection. Median pretreatment viral loads were higher in the relapsing group (80,150 copies/106 leukocytes) than in the nonrelapsing group (5500 copies/106 leukocytes; P=.007). The relapsing group also had persistent detectable viral DNA (median, 5810 copies/106 leukocytes) after treatment, whereas it was undetectable in the nonrelapsing group (P<. 0001). Primary CMV infection (seronegative recipients of seropositive organs, D+R-) was an independent marker for CMV relapse (P=.03), and these patients had higher pre- and posttreatment viral loads than did non-D+/R- patients (P<.0001 and P=.0014, respectively). CMV DNA load is a useful marker for individualizing antiviral treatment of CMV infection in solid organ transplant recipients.

Although our study demonstrates the adequacy of all blood compartments for CMV DNA quantification, the higher sensitivity of WB and its yield of higher CMV DNA render it an optimal sample for monitoring CMV DNA load during CMV disease in immunocompromised patients.

We investigated the effect of beta-herpesviruses on allograft failure and mortality, hepatitis C virus (HCV) replication, and liver histologic characteristics among 92 HCV-infected liver transplant recipients. Reactivation of cytomegalovirus (CMV) but not of human herpesvirus 6 (HHV-6) was independently associated with allograft failure and mortality (risk ratio, 3.71; 95% confidence interval, 1.64-8.39); allograft failure and mortality was observed in 48% of patients with CMV disease, 35% of patients with subclinical CMV infection, and 17% of patients without CMV infection (P=.0275). CMV reactivation was highly predictive of mortality (P<.001), regardless of whether it remained subclinical or evolved into CMV disease. Patients with CMV disease had a higher fibrosis stage (P=.05) and had a trend toward a higher hepatitis activity index (P=.10) and HCV load (P=.10) at 16 weeks after liver transplantation. The pathogenesis of HCV is influenced by its interaction with CMV but not with HHV-6.

Human herpesvirus (HHV)-6 and HHV-7 are increasingly being recognized as emerging pathogens among transplant recipients. Using quantitative polymerase chain reaction assays, we demonstrate the presence of HHV-6 and/or HHV-7 in 18 of 20 episodes of clinically presumed or microbiologically confirmed cytomegalovirus (CMV) infection. Seventeen (89%) of 19 microbiologically confirmed cytomegalovirus (CMV)-infected patients had concomitant HHV-6 variant B (47%) and/or HHV-7 (63%) infection. The degree of HHV-6 coinfection was significantly correlated with hyperbilirubinemia while HHV-7 coinfection demonstrated a non-significant trend toward cytopenias. In one of the 20 episodes described herein, the 'viral syndrome' was due solely to HHV-7 infection; clinical and virological response was observed during intravenous ganciclovir therapy in this patient. While this study emphasizes the significance of HHV-6 and/or HHV-7 coinfection during episodes of CMV infection, it significantly highlights the novel observation of the causal role of HHV-7 (in the absence of HHV-6 and CMV) in a clinical illness presumed to be caused CMV. Thus, HHV-7 (and HHV-6) should be considered as a pathogen (or copathogen) in the viral syndromes following organ transplantation.