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Background Chronic infection with hepatitis E virus (HEV) has recently been recognized in immunocompromised or immunosuppressed individuals. Case Report We report a case of concurrent HEV and human herpes virus-6 (HHV-6) infection, documented by serum HEV RNA and HHV-6 DNA, in an orthotopic liver transplant (OLT) recipient in the United States, where HEV genotype 3 infection, although prevalent, is considered to be self-limited and almost always asymptomatic. The coinfection was accompanied by elevated serum aminotransaminases, liver biopsies demonstrating chronic hepatitis, and the presence of HEV RNA in the tissue. After lowering of immunosuppressive therapy and 2 courses of valganciclovir, sequential clearance of the viruses and normalization of the serum aminotransaminases were observed. Conclusions HEV infection can lead to chronic hepatitis in OLT recipients, and evaluation of this virus should be considered in immunosuppressed individuals with unexplained liver test abnormalities.

The monitoring of herpesvirus infection plays a central role in lung transplantation (LT). Herein we evaluated the prevalence of human cytomegalovirus (HCMV), human herpesvirus-6 (HHV-6), human herpesvirus-7 (HHV-7), and Epstein-Barr Virus (EBV) DNA in bronchoalveolar lavage (BAL) and transbronchial biopsy (TBB) specimens from LT patients. We associated the findings with the occurrence of interstitial pneumonia, acute rejection, or organizing pneumonia. Viral DNA was detected using real-time polymerase chain reaction (PCR) on 76 paired samples (BAL and TBB) from 27 patients who were receiving a universal combined prophylaxis (cytomegalovirus [CMV] immunoglobulin [Ig] + gancyclovir or valgancyclovir). Histopathological analysis was performed in accordance with the International Society for Heart and Lung Transplantation (ISHLT) criteria. Overall, HCMV results were positive in 25/76 (32.9%) specimens (BAL and/or TBB); HHV-6 in 16 (21.1%); HHV-7 in 40 (52.6%); and EBV in 13 (17.1%). Interstitial pneumonia was diagnosed in 6/76 (7.9%) cases: 5 (83.3%) were positive to HCMV (combined specimens; P < .0001); 5 (83.3%) to HHV-7; and 2 (33.3%) to EBV. An acute rejection episode was diagnosed in 19/76 (25%) cases: 7 (36.8%) were positive to HCMV; 5 (26.3%) to HHV-6; 10 (52.6%) to HHV-7, and 3 (15.8%) to EBV. No significant association was observed between virus detection or load and acute rejection. Organizing pneumonia was diagnosed in 4/76 (5.3%) cases: 1 (25%) positive to HCMV; 4 (100%) to HHV-6 (P < .05); 2 (50%) to HHV-7; and none to EBV. In conclusion, the prevalence of HCMV tended to be lower than that reported in the literature, confirming the importance of universal combined prophylaxis. HCMV was a relevant agent for interstitial pneumonia; although the small numbers limit the statistical analysis, our data did not support an association between herpesviruses and acute rejection episodes, whereas the role of HHV-6 in the pathogenesis of organizing pneumonia deserves further study. Viral detection on TBB could represent an adjunctive tool to complement that on BAL.

Human herpesvirus-6 (HHV-6) is an opportunistic viral pathogen of emerging clinical significance in immunocompromised patients. We performed a seroepidemiological survey to test the relation between seroprevalence among donors and recipients for HHV-6 at three endpoints. Before transplantation sera obtained from cadaveric donors and from potential recipients were tested for IgG antibodies against HHV-6 using an enzyme-linked immunoassay. The group of recipient sera, including samples obtained before as well as 2, 4, 12, and 48 weeks after transplantation, were tested for anti-HHV-6 IgM antibodies using an indirect immunofluorescence assay. The statistical analysis was performed with the Cox proportional hazards models. The HHV-6 seronegative group (n = 11) compared with the HHV-6 seropositive group (n = 109) showed twice the risk of HHV-6 IgM seroconversion (RR = 2.24; P < .04), with a greater risk of fever, namely 3.8, which was on the verge of statistical significance. The opposite trend toward an association with acute rejection episodes was observed among HHV-6 seronegative patients (RR = 1.81). The presence of IgG antibody in the sera of donors to IgG seropositive recipients had no association with the occurrence of IgM seroconversion. In contrast, IgM antibodies to HHV-6 appeared in four of five seronegative patients who received allografts from IgG seropositive donors. These preliminary data suggest that the effects seem to be the consequence of HHV-6 transmission through a renal allograft.

Human herpesvirus (HHV)-6, comprised of HHV-6A and HHV-6B, belongs to the betaherpesviruses that infect 95%–100% of humans. Primary infection, known as exanthema subitum, occurs in early childhood. Reactivations of latent HHV-6, mostly HHV-6B, are common after liver transplantation. The vast majority of them are asymptomatic; in a minority of cases, the virus may infect the liver transplant, causing graft dysfunction or hepatitis. An association between hepatic HHV-6 infection and indeterminate acute liver failure (ALF) has been shown, but the causality is not clear because of the ubiquitous nature of HHV-6. We have previously observed HHV-6B antigens in the explanted livers of most patients (80%, n = 32) transplanted with ALF of unknown cause, whereas it was not observed among those with ALF of known cause. After transplantation, half of the patients with pretransplant HHV-6 infection (9/18) developed recurrences. The aim of this study was to investigate their long-term course (9–14 years). Half of the patients with pretransplant HHV-6 developed recurrences. Two also showed cytomegalovirus (CMV) hepatitis, whereas none of the other patients demonstrated intrahepatic CMV. During the 9 years or more of follow-up, 1 graft and 2 patients were lost in both groups (HHV-6 recurrence/HHV-6-negative patients). The reasons for graft loss were hepatic arterial thrombosis and portal venous thrombosis. In addition 2 patients died in the HHV-6 recurrence group, one because of rethrombosis of hepatic artery (day 460) and one with a functioning transplant (4.5 years after transplantation). In the control group 1 patient died at 1.5 years and 1 at 10 years after liver transplantation because of pneumonia. HHV-6 relapse was common in ALF patients after transplantation. However, HHV-6 did not cause liver failure and had no significant long-term effect on survival.

Herpes virus reactivation is of increasing interest as we aim to decrease morbidity and mortality in the pediatric renal transplant population. We previously reported increased reactivation of HHV-6 and Epstein Barr virus (EBV) with anti-thymocyte globulin/ALG induction therapy. HHV-6 reactivation and de novo infection has been monitored in 31 consecutive pediatric renal transplant patients receiving antibody induction with Simulect. Human Herpes virus-6 (HHV-6) was correlated with EBV reactivation and de novo infection rates, allograft function at 1 year, donor source and number, and patient age and gender. One HHV-6 de novo infection was associated with an early grade II rejection that was steroid resistant but ATG/ALG responsive. Sixteen of 31 (54.8%) patients had HHV-6 reactivation during the first year and eight patients had a prior reactivation profile before transplant. Thirteen patients (41.9%) were naïve to EBV infection prior to transplant with evidence of primary infection in 11 of 13 patients between 6 weeks and 1 year posttransplant. EBV reactivation was noted in four patients with past immunity to EBV. IgM Ab to EBV or HHV-6 during the first year posttransplant did not correlate with risk of rejection during the first year or graft function one year posttransplant. The only patient with positive HHV-6 IgM Ab in the first posttransplant month was a de novo infection in a 2-year-old boy who was naïve for HHV-6 at the time of transplant. Simulect appears safe in pediatric renal transplant with low risk of HHV-6 or EBV infection in the first 1 to 2 months posttransplant.

Varicella is a well-known contagious disease of childhood that can also affect both immunodepressed and immunocompetent adults. The present observations concern a previously healthy adult patient who presented with a fulminant hepatitis evolving in multiorgan failure (MOF), associated with an atypical papulo-ethemateous cutaneous rash without fever. An hepatic biopsy showed massive necrosis. Because of the persistent MOF and severe hemodynamic instability, total hepatectomy was performed as a bridge to urgent liver transplantation (OLT). Despite temporary improvement, the patients condition progressively deteriorated and he died 11 hours after the hepatectomy, i.e. 7 days after admission to the intensive care unit. High viral loads of varicella zoster virus (VZV) and human herpes virus 6 (HHV6) were demonstrated in the blood and in DNA at post mortem examination of the liver, kidneys, lung, and heart. We hypothesize that VZV infection may occasionally occur in immunocompetent patients due to extremely virulent strains that can be rapidly fatal. The clinical influence of simultaneous infection with HHV6 is not clear. Moreover, the role of a previous steroid treatment as a trigger for a temporary immunodepressed state must be considered. The diagnosis of liver disease from VZV should always be clinically suspected in the presence of concurrent atypical skin lesions and a temporarily immunocompromised state. Therapy with acyclovir was ineffective in our patient. Based on the wide spectrum of VZV infections, fulminant MOF in immunocompetent adults must raise the possibility of VZV with simultaneous HHV6 infection with early listing of the patient for a urgent OLT, possibly with a total hepatectomy as a bridge, due to the therapeutic uncertainty of medical treatments.

In addition to cytomegalovirus (CMV), activation of other betaherpesviruses, especially human herpesvirus 6 (HHV-6), has been reported in liver transplant patients. The purpose of this study was to investigate the posttransplant HHV-6-DNAemia in relation to CMV-DNAemia in liver transplant patients. Thirty-one adult liver allograft recipients were regularly monitored for CMV and HHV-6 during the first 3 months after transplantation. For the diagnosis of CMV infections, pp65-antigenemia assay and quantitative DNA-PCR were used. HHV-6 was demonstrated by using quantitative DNA-PCR and HHV-6 antigenemia test. Altogether 253 blood specimens of 31 recipients were analyzed. In addition, CMV and HHV-6 specific antigens were demonstrated by immunohistochemistry in liver biopsy specimens in the case of graft dysfunction. Thirteen patients (40%) developed a clinically significant CMV infection, at a mean of 33 days (range 5 to 62 days) after transplantation and were treated with intravenous ganciclovir. The peak viral loads of these symptomatic CMV infections were high (CMV-DNA 34210 +/- 37557 copies/mL plasma). Six additional asymptomatic patients demonstrated significantly lower CMV-DNAemia levels (1020 +/- 1008 copies/mL, P.05), and were not treated. Concurrently with CMV, HHV-6 DNAemia and antigenemia were detected in 17 of 19 patients, mean 11 days (range 6 to 24 days) after transplantation. HHV-6 appeared prior to CMV in most cases (12 of 17). However, the peak viral loads were low (HHV-6-DNA1500 copies/mL blood), even in the five patients who demonstrated HHV-6 antigens on liver biopsy. All CMV infections were successfully treated with ganciclovir and the CMV DNAemia/antigenemia subsided. HHV-6 also responded to the antiviral treatment, but more slowly and less clearly. In conclusion, HHV-6 activations were common and usually associated with CMV infection in liver transplant patients. Further investigation of the clinical significance of HHV-6 DNAemia/antigenemia is necessary.

Objective Human herpesvirus (HHV) 6 infections and reactivation are emerging factors in neurology. This study aimed to verify the presence of encephalitis associated with HHV-6 positivity by antigenemia or polymerase chain reaction (PCR) in liver transplant recipients. Methods We analyzed the medical records and laboratory results of 20 recipients with antigenemia or a positive PCR for HHV-6. The range of the transplantation dates was September 2006 to March 2010; the period of the medical records was from the date of transplantation to 1 year thereafter. Encephalitis was diagnosed by these symptoms: fever, mening, signs, seizures, dysphasia, visual and hearing impairment, or sensory and motion alterations. “Possible encephalitis” was considered when the patients had at least 2 of the symptoms. PCR or antigenemia for HHV-6 was not performed with central nervous fluid. The correlation between HHV-6 infection and encephalitis was evaluated with the use of descriptive statistical tests. Results Symptoms associated with encephalitis occurred in 7/20, patients (35%): 5/20 with fever and 4/20 with mental confusion. Involuntary movements were present in 1 case. The symptoms appeared with in the first 10 days in 6/20 patients and lasted for 1 year. Conclusions This study showed that symptoms associated with encephalitis occurred in a considerable number of patients with positive PCR and/or antigenemia for HHV-6 after liver transplantation. This correlation needs retrospectie and prospective studies to determine the specific association.

Cytomegalovirus (CMV) and human herpesvirus-6 (HHV-6) reactivation after transplantation put patients at an increased risk of graft rejection mainly among those who receive organs that are positive in their donor biopsies. The aim of this study was to investigate the presence of CMV and HHV-6 DNA in liver biopsy specimens from the donors and from their grafts for correlation with rejection after transplantation. We followed 41 liver transplantation patients whose samples were evaluated using nested-polymerase chain reactions (N-PCR). Twenty-one (51%) of the 41 studied patients experienced rejection; 4/21 (19%) were CMV positive in the donor biopsy specimens and remained positive; another 5 subjects became positive. The patients who received organs from donors with biopsies positive for CMV demonstrated a trend to develop graft rejection after transplantation (Fisher's exact test [P = .0591] with significant results on univariate and multivariate analysis [P = .042]). Eight of the 21 who experienced rejection episodes were HHV-6 positive in the donor biopsy but there was no statistical significance CMV DNA diagnosed in liver donor biopsies remained positive posttransplantation in liver biopsy recipients; it was considered a tendency to develop acute cellular rejection after transplantation.

Background. Human herpesvirus (HHV) 5 and 6 remain latent after primary infection and can be reactivated after immunosuppression for organ transplantation. An association between HHV-5 and HHV-6 has been reported in liver transplant patients. The coinfection is associated with clinical manifestations and graft dysfunction. Objective. The aim of this study was to monitor herpesviruses in liver transplant recipients to better understand issues involving coinfection with HHV-5/6 and correlations with acute cellular rejection episodes and bacterial infections. Methods. Forty-five adult liver transplant patients of median age 47 years (range, 18‐66), gave blood samples and liver biopsies in the first 6 months after their surgeries. Viremia was detected with the use of nested PCR and antigenemia; the Banff classification was used to detect allograft rejection. Results. IgG positive for HHV-5 was observed in 94% of subjects whose main indication (67%) for transplantation was hepatitis C. Twenty-three (51.1%) displayed cytomeg virus (CMV) infections and 12 (26.7%) HHV-6 infection. There were 6 patients (13.3%) with HHV-5/6 coinfections. Eighteen of the 23 patients had CMV disease, showing a strong correlation between a positive test and CMV disease; 6 displayed an acute cellular rejection episode in the same period ( 2 6.62; P .03). Four out of 6 patients who displayed coinfections (HHV-5/6) had concomitant bacterial infections; 3/6 experienced graft rejection episodes. During follow-up, 1 patient had HHV-6 infection diagnosed as encephalitis followed by fever on the 24th day after surgery. The median 32 days for HHV-6 detection by nested PCR positivity was shorter than 38 days for HHV-5. Conclusions. HHV-5/6‐infected patients displayed more allograft rejection episodes, coinfections, and concomitant bacterial infections, besides an higher risk for CMV disease.

Human herpesvirus (HHV)-6, HHV-7, and cytomegalovirus (CMV) that remain latent after primary infection can be reactivated during immunosuppression following organ transplantation in liver transplant recipients. The aim of this study was to monitor active infections for HHV-6, HHV-7, and CMV among adult liver transplantation recipients using antigenemia detected by an immunoperoxidase staining. Twenty-eight adult liver transplant patients were monitored using antigenemia in blood samples obtained at the time of transplantation, as well as weekly in the first month and once a month for 6 months. Of these patients, 28.5% showed positive CMV antigenemia; 39.2%, HHV-6 antigenemia; and 14.2%, HHV-7 antigenemia. The detection of the three viruses was considered to be independent of one another (P > .05). The results described above showed that few patients remain free of beta herpesviruses after liver transplantation. Most patients were infected sequentially and not concurrently. Antigenemia has been considered useful to detect active HHV-6 and HHV-7 infections. Antigenemia can be more efficiently interpreted when compared with polymerase chain reaction results, although other studies are necessary to establish the reference of HHV-6 and HHV-7 antigenemia.

One hundred two recipients of hematopoietic stem cell transplants (HSCTs) 45, from siblings and 57 from matched unrelated donors, were followed for cytomegalovirus (CMV), human herpes virus (HHV) 6, and Epstein-Barr Virus (EBV) reactivation by quantitative polymerase chain reaction in the context of immunologic reconstitution and posttransplantation complications. CMV, EBV, and HHV6 DNA copies (100 copies/10(5) cells) were detected in 34%, 27%, and 26% of patients, respectively. The presence of 100 copies of EBV or CMV was associated with posttransplant complications: 29/66 versus 6/36 (P.01) or 24/66 versus 4/36 (P=.01). CMV reactivation was more frequent among patients with acute graft-versus-host disease grade≥I: 17/35 versus 18/67 (P.05). Older patient age of adults16 year (2/16 versus 33/86; P.05) and, to a lesser extent, CMV IgG positivity before HSCT (34/84 versus 1/10; P=.08) or an HLA-mismatched graft (9/16 versus 26/86; P=.08) constituted risk factors for CMV reactivation, which resulted in a higher rate of bacterial pneumonia (7/11 versus 28/91; P=.04). EBV reactivation risk was associated with donor EBV IgG seropositivity (28/84 versus 0/10; P=.03) and donor female gender (18/47 versus 10/55; P=.03). In contrast to EBV and CMV, EBV reactivation itself was associated with encephalitis (5/8 versus 23/94; P=.013), which was also seen as a trend among HHV6 reactivations (8/8 versus 46/94; P=.08). Multivariate analysis demonstrated that these factors play independent roles in the reactivation of the investigated herpes viruses.

BACKGROUND: Cytomegalovirus (CMV) and Epstein-Barr virus (EBV) are the major causes of graft failure and posttransplantation mortality among small bowel and multivisceral transplantations (SB/MVT). Little is known about human herpes virus 6 (HHV-6) infections in transplant recipients. STUDY PURPOSE: The purposes of this study were to analyze the clinical relevance of CMV, EBV, and HHV-6 infections after small bowel transplantation and to establish whether routine monitoring for HHV-6 infection should be recommended for the prevention of severe complications in this population. METHODS: Ten adult patients were monitored based on CMV, EBV, and HHV6 DNA quantifications in blood and biopsy tissue samples. Three patients were monitored for at least 5 months (early period) and 7 patients were monitored for 1 to 5 years after transplantation (late period). RESULTS: In the early period, despite prophylaxis all 3 patients developed symptomatic CMV infections: 1 fever/diarrhea, 1 enteritis and rejection, as well as 1 fever and pneumonia. Only 1 patient developed EBV and HHV-6 infections. The average time of onset of CMV infection was 3 months after transplantation and only 24 days for HHV6 infection. In the late period, of the 7 SB/MVT recipients only 1 developed an EBV infection at 2 years after transplantation. No CMV or HHV-6 infections were identified in any patient. CONCLUSIONS: CMV infection is a major cause of organ disease and rejection in the early period after transplantation. EBV infection in adult recipients must be considered also in the late period, particularly in association with severe immunosuppression. Because HHV-6 infection occurs earlier than CMV/EBV, it may serve as an indicator for more intense virological surveillance.

Cytomegalovirus (CMV), Epstein-Barr virus (EBV), and human herpesvirus-6 (HHV-6) cause symptomatic diseases in liver transplant recipients. The loads of these viruses, the associations between viral DNAemia, serologic status, and acute rejection reactions were investigated in a group of 17 juvenile and 17 adult recipients of living donor liver transplantation (LDLT) for a median of 8 weeks posttransplantation. At least 1 plasma sample from 15/34 (44.1%) patients was positive for CMV DNA. For most of the CMV-positive patients, the CMV DNA appeared in the second week of LDLT, and disappeared by the eighth week. A minimum of 200 EBV DNA copies/mug peripheral blood mononuclear cell DNA (defined as positive for EBV) was detected in 5/34 (14.7%) patients, and the number of EBV-positive children was significantly greater than the number of EBV-positive adults. In most of the EBV-positive patients, the EBV loads increased after 4 weeks posttransplantation. Plasma HHV-6 was detected in 7/34 (20.6%) patients. HHV-6 DNA appeared for a short period from the second week of LDLT. In addition, 8 of the 19 virus-positive recipients carried 2 viruses, with the combination of CMV and HHV-6 being the most frequent. Serologic status seemed to be an important factor for all 3 viral infections. The rate of acute cellular rejection was not significantly higher in the CMV-, EBV-, or HHV-6-positive groups. Simultaneous monitoring for 3 herpesviruses revealed the impact of these viruses on LDLT recipients.

In order to know the influence of ganciclovir (GCV) prophylaxis on cytomegalovirus (CMV) human herpesvirus (HHV)-6 and HHV-7 replication in renal transplant recipients, three groups were studies: 54 patients without GCV; 29, with short-term GCV prophylaxis (less than 30 days); and 51, with long-term GCV prophylaxis (more than 60 days). CMV viremia was more prevalent in the first group (74%, 55%, and 29%, respectively), but CMV replication was also found in 14 patients during therapy, in the other two groups. The antiviral did not affect the prevalence of HHV-6 (67.2%) or HHV-7 (76%), but HHV-6 viremia appeared later (42 +/- 31 vs 21 +/- 25/38 +/- 29 days posttransplant) and was shorter (29 +/- 30 vs 62 +/- 34/41 +/- 33 days) among patients with long-term GCV prophylaxis. On the other hand, CMV viremia was longer when HHV-6 replication was present (40 +/- 25 days vs 18 +/- 16 days). In addition, HHV-7 DNA was detected in all patients with CMV disease.

Herpesviruses, including human herpesvirus-6 (HHV-6), reactivate and have the potential to be pathogenic in immunocompromised patients. Little information is available regarding the correlation between immunosuppressive therapy and HHV-6 seroconversion after organ transplantation. Serum samples obtained from 120 kidney and kidney/pancreas transplant recipients were tested to explore the potential risk factors for developing HHV-6 infection including types of immunosuppression and induction/rejection therapy. Stored serum samples obtained prior to and at the 2nd, 4th, 12th and 48th weeks after transplantation were tested for anti–HHV-6 immunoglobulin (Ig)M antibodies using indirect immunofluorescence assay. Prior to transplantation and 48 weeks after transplantation the sera were additionally tested for anti–HHV-6 IgG using enzyme-linked immunoassay. Ninety-one percent of 120 recipients were HHV-6 IgG-positive before transplantation. One hundred seven of 120 patients were anti–HHV-6 IgM-negative before transplantation. Primary/secondary HHV-6 seroconversion occurred in sera of 46.6% of these 107 patients. HHV-6 seroconversion most frequently occurred 2 to 4 weeks after transplantation. There was no significant relationship between HHV-6 seroconversion and the treatment with methylprednisolone (MP). The incidence of HHV-6 seroconversion was significantly higher in subjects who were treated with the regimens including Daclizumab or Sirolimus as compared with those who were on other protocols. HHV-6 seropositivity in the Polish population of organ transplant recipients is very high. We demonstrated a trend toward association of HHV-6 seroconversion with type of immunosuppressive therapy.

GRAFT-VERSUS-host disease (GVHD) is a relatively common complication that appears after bone marrow or hematopoietic stem cell transplantation. The humanized anti-interleukin 2 receptor antibody (daclizumab) has been used successfully in the treatment of GVHD. GVHD is an increasingly common complication of liver transplantation. Two hundred fifty one liver transplantations have been performed in our hospital; only two of these patients had GVHD. We hereby describe one of these patients, who was successfully treated with daclizumab after previous authorization issued by the Spanish Ministry of Health (as daclizumab is currently not approved for liver transplantation in Spain).

Purpose To analyze the incidence and relevance of viral infections after intestinal transplantation (ITx) without specific antiviral prophylaxis. Methods Eleven patients (median age 34 years; range 26 to 58 years) who underwent ITx received no CMV/EBV prophylaxis but rather preemptive treatment. Viral monitoring for CMV or EBV polymerase chain reactions (PCR) in peripheral blood and graft biopsies, for HHV6-, and HHV7-PCR; for adeno-/rotavirus antigen and serology was performed based on clinical indications. Results Median time under risk was 19 months (range 2 to 39). CMV: The donor (D)-to-recipient (R) status prior to ITx was: D+/R+ (4); D+/R− (3); D−/R− (2); D−/R+ (2). Eight patients showed no positive CMV-PCR. Three episodes of tissue invasive CMV disease occurred in two patients. There were two asymptomatic CMV infections but no episodes of CMV disease. None of the R(−) recipients developed CMV infection or enteritis irrespective of the donor status. EBV: Four patients experienced six episodes of transient significant EBV-viremia. Two patients developed EBV enteritis concurrently with CMV enteritis during acute rejection. There were no PTLD. CMV and EBV enteritis only occured during or immediately after steroid and OKT3 therapy. None of the patients developed significant HHV6 and HHV7 infection or viremia. There was one episode of adeno- and rotavirus enteritis. Conclusions Despite witholding specific antiviral prophylaxis against CMV and EBV, we observed no such infections in 60% to 80% of patients. Donor-recipient matching regarding CMV was not predictive for the occurence of CMV-related complications. HHV6 and HHV7 have not contributed to posttransplant morbidity.

CYTOMEGALOVIRUS (CMV) is an important opportunistic infection after heart transplant. The new human herpesvirus, types 6 and 7 (HHV6, HHV7) are two lymphotropic herpesviruses, which, like CMV, have the potential to be pathogenic in immunocompromized individuals. Recent studies suggest that both viruses can cause clinical illness after transplantation. These viruses may be a risk factor for CMV disease in posttransplant patients, possibly through a direct interaction or through a general immunomodulatory effect. However, the pathogenic potential and the clinical features have not been defined. To evaluate the reactivation of HHV6 and HHV7 after heart transplantation and their implication in the cytomegalovirus disease (CMVD), 42 unselected heart transplant patients were studied.