| Research Abstract |
Although it has been demonstrated that human herpesvirus 6 (HHV-6) infection occurs almost half of the hematopoietic stem cell transplant (HSCT) recipients, and might be associated with several clinical manifestations including acute graft versus host disease, mechanisms of viral reactivation remains unclear. To explore the mechanisms of HHV-6 reactivation in HSCT recipients, we sequentially monitored serum proinflamatory cytokines (IL-G, TNF-α, and IL-1β) levels and HHV-6 infection (viral isolation and serological assay) in the 24 pediatric patients after HSCT. Of the patients, 14 (58.3%) developed HHV-6 infection, and 9 (37.5%) developed HHV-6 viremia around 2 weeks (days 0, 14, 15, 14, 16, 15, 13, 21, and 22) after transplantation. The mean levels of three cytokines (IL-6, TNF-α, and IL-1β), which were measured at days 0, 7, 14, and 28 of post-transplant, were compared between patients with HHV-6 infection and those without HHV-6 infection. IL-6 levels were significantly higher in patients with HHV-6 infection than in those without HHV-6 infection at day 7 (54.8 vs 16.3 pg/ml; P=0.0272), 14 (44.2 vs 0.4 pg/ml; P=0.0002), and 28 (18.8 vs 4.4 pg/ml; P=0.0137). In addition, TNF-α level was significantly higher in patients with HHV-6 infection than in those without HHV-6 infection at day 14 (13.1 vs 3; P= 0.023). In other time points, there was no significant difference of mean IL-6 and TNF-α levels between. patients with HHV-6 infection and those without HHV-6 infection. Low level of IL-16 was detected in small number of serum samples, and there was no significant difference between patients with HHV-6 infection and those without HHN-6 infection. These results suggest that proinflamatory cytokines, in particular IL-6 and TNF-α, may play an important role in the pathogenesis of HHV-6 infection after HSCT, and may be a useful predictor for HHV-6 :infection.
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