Age, median (range, y) 5.9 (0.4-17.6) 6 (1.8-17.9) 6.03 (0.7-18) 6.5 (0. [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14] [15] [16] [17] [18] .84
Male 
We retrospectively analyzed viral infections and the outcome of one hundred and seventy-one pediatric patients (median 7.38 years) who underwent allogeneic HSCT from January 2014 to September 2016.
Patients were divided into four subgroups: patients transplanted from MRD (n = 71), 10 of 10 HLA allele-MUD (MUD1; n = 29), 9 of 10 HLA allele-MUD (MUD2; n = 40), and haploidentical donors (n = 31).
Patients' characteristics were summarized in Paired-sample t test was used for the comparison of dependent variables. A two-tailed P value <.05 was considered statistically significant.
Kaplan-Meier method was used for survival analysis.
One hundred and seventy-one pediatric patients undergoing HSCT
were enrolled to study. The median duration of follow-up was 14 months (range 1-31 months). The main diagnosis, HLA disparity, donor type, conditioning regimen, the use of corticosteroids and ATG, the median CD34+ cells of the grafts, engraftment days of neutrophils, platelets, and lymphocytes, lymphocyte count at day 100 and the day lymphocyte count >1000/mm 3 , and the existence of acute and chronic GVHD according to donor type are summarized in Table 1 .
were achieved about 5 to 10 days earlier in patients receiving haplo-HSCT than in patients receiving MRD or MUD HSCT, but these differences were statistically not different ( Table 1 ). The lymphocyte count at day 100 and the day when the lymphocyte count was greater than 1000/mm 3 did not significantly differ between the four groups (Table 1) . Immunophenotypic analysis reveals a progressive but slow increase in lymphocyte subset counts from day +30 through later Table 2 . Tables 4 and 5 . Overall survival was influenced with having one or multiple viral infection (P = .04 and P = .0008). TRM at day 100 was not statistically significant between four groups, but TRM at the end of follow-up was found statistically significant (P < .0001). This significance was especially prominent between MRD and MUD1/MUD2/ haplo-transplantations (P < .0001, P = .008, and P = .03). Comparison of overall survival at the end of follow-up between the four groups was associated with significantly better survival in the MRD group (log rank test, P < .0001).
Viral infections due to impaired immune reconstitution remain a cause of morbidity and mortality in HSCT patients. The incidence of viral infections can be the best indicator of immune recovery. This study, with 171 pediatric patients, is the second largest study, which reports the incidence of virus infections in children following allogeneic HSCT.
We found that viral infections are especially common in the first of our knowledge, our study is the only study that compared the viral incidence between haplo-HSCT and MRD/MUD HSCT. We detected the incidence of CMV reactivation in 28.2% ofMRD patients but more than 60% of haplo-and MUD1/MUD2 HSCT recipients were positive for CMV reactivation. This difference can be explained with ethnic and geographical differences in CMV seroprevalence in Turkish population. 10, 11 In our country, the seroprevalence rates in the age groups of 1-6, 7-14, and 14-49 years were detected as 82%, 92%, and 97.8%, respectively. 11
BK virus was the second most seen virus in our study. BK virus is more frequent in the presence of MUD, haplo-HSCT, cord blood transplantation, GVHD, advanced age, and persistent thrombocytopenia. [12] [13] [14] We also found BK virus frequently among the recipients of MUD1, MUD2, and haplo-HSCT than those of MRD grafts.
ADV is increasingly recognized as an important pathogen in the recipients of allogeneic HSCT. 15 The reported mortality of patients with sustained high ADV DNA level in plasma is remarkably high, varying from 20% to 80% in different studies. 16, 17 In our study, 16.1% of haplo-HSCT patients, 15% of MUD2 HSCT patients, and 6.9% of MUD1 HSCT patients developed ADV infection.
PTLD, which occurs in <1% of the patients after HSCT. 18 We found nine patients who showed EBV reactivation. Interestingly, we detected the lack of PTLD, as reported also by Kanakry et al 19 