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Dynamic EBV gene loads in renal, hepatic, and cardiothoracic transplant recipients as determined by real‐time PCR light cycler
Author(s) -
Leung E.,
Shenton B.K.,
Green K.,
Jackson G.,
Gould F.K.,
Yap C.,
Talbot D.
Publication year - 2004
Publication title -
transplant infectious disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.69
H-Index - 67
eISSN - 1399-3062
pISSN - 1398-2273
DOI - 10.1111/j.1399-3062.2004.00073.x
Subject(s) - medicine , asymptomatic , viral load , real time polymerase chain reaction , transplantation , post transplant lymphoproliferative disorder , gastroenterology , mononucleosis , taqman , renal transplant , kidney transplantation , immunology , epstein–barr virus , virus , gene , biology , biochemistry
Background: Epstein–Barr virus (EBV) is recognised as one of the causative agents for most cases of post‐transplant lymphoproliferative disease (PTLD). Elevated levels of EBV DNA are known to be associated with the onset of PTLD, but little information is available regarding how EBV loads change with time in asymptomatic transplant recipients following transplantation. Our aims were to study the trend of EBV loads in renal (RTx), hepatic, and cardiothoracic transplant recipients and to compare their EBV loads with other healthy and patient controls. Methods: A prospective study was performed using a real‐time TaqMan polymerase chain reaction technique to measure EBV DNA loads from three types of organ transplant recipients and haemodialysis patients (HD). Their results were then compared with those from the healthy controls (HC); monospot test negative (MN−) and infectious mononucleosis positive (IM+) patients; patients who were previously treated for PTLD (pPTLD); those who were currently diagnosed to have PTLD (PTLD+); and patients who had a stable renal, hepatic, or cardiothoracic graft for more than a year. Results: Post‐transplant EBV loads were significantly higher than the pre‐transplant levels. Asymptomatic transplant recipients were differentiated from the PTLD+group at 600 genome copies of EBV/μg DNA, and from IM+group at 100 genome copies. Both HC and MN− groups had significantly lower EBV loads than the three transplant groups. The dynamic change of EBV loads in RTx was greater in the first post‐transplant month when compared with the HD group. All transplant recipients had transient rises of EBV loads whereas EBV load continued to rise in one suspected PTLD patient. Conclusions: Asymptomatic transplant recipients had higher baseline post‐transplant EBV levels than the non‐transplant and MN− groups. The rising post‐transplant EBV load in these transplant recipients did not seem to be sustained for longer than 2 weeks. However, in a PTLD+patient the rising EBV load continued over a period of 4 weeks. Hence, the dynamic pattern of EBV loads is more important than absolute EBV DNA measurements alone in identifying those who might go on to develop PTLD.