BK virus (BKV) quantification in urine samples of bone marrow transplanted patients is helpful for diagnosis of hemorrhagic cystitis, although wide individual variations exist

Abstract Background: Hemorrhagic cystitis (HC) in allogeneic bone marrow transplanted (BMT) patients is associated with BK virus (BKV) reactivation manifested as BK viruria. However, since 77–90% of all adult BMT patients excrete BKV, viral reactivation alone cannot be responsible for HC. Recently, a significant overrepresentation of C→G mutations in the Sp1 binding site in the non-coding control region (NCCR) of BKV was shown to be present in HC patients and absent in non-HC patients. Objectives: We aimed to investigate if this mutation resulted in excessive BKV excretion in HC patients. Study design: A Real-Time PCR was developed and used to quantify BKV in urine samples from 21 patients with HC, with and without the mutations, as well as from patients without HC. Results: Quantification of BKV was successful in 18 of 21 urine patients (six with and six without C→G mutations) and six patients without HC. A mean of 3.0×10 6 BKV copies/μl was detected in urine samples of HC patients with C→G mutations, compared to a mean of 1.5×10 6 BKV copies/μl in HC patients without C→G mutations and a mean of 1.0×10 6 BKV copies/μl in patients without HC. The obtained differences were however not statistically significant, due to one individual non-HC patient with an extremely high BKV copy number. Nevertheless, while 50% of the samples in the HC groups expressed 1×10 6 copies/μl or more, only one of the samples in the non-HC group contained a virus quantity higher than 5×10 5 copies. Conclusions: Although we could not confirm that the C→G mutations in the Sp1 site of BKV were responsible for an increased viral load in patients with HC, our data suggest that levels of BKV above 10 4 copies/μl may indicate a risk for HC.