| Summary: | Background: Hemorrhagic cystitis (HC) in allogeneic bone marrow transplanted (BMT) patients isassociated with BK virus (BKV) reactivation manifested as BK viruria. However, since 77–90% of alladult BMT patients excrete BKV, viral reactivation alone cannot be responsible for HC. Recently, asignificant overrepresentation of C→G mutations in the Sp1 binding site in the non-coding controlregion (NCCR) of BKV was shown to be present in HC patients and absent in non-HC patients. Weaimed 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 withHC, with and without the mutations, as well as from patients without HC.Material and method: A Real-Time PCR was developed and used to quantify BKV in urinesamples from 21 patients with HC, with and without the mutations, as well as from patients withoutHC.Results: Quantification of BKV was successful in 18 of 21 urine patients (six with and six withoutC→G mutations) and six patients without HC. A mean of 3.0×106 BKV copies/μl was detected inurine samples of HC patients with C→G mutations, compared to a mean of 1.5×106 BKV copies/μl inHC patients without C→G mutations and a mean of 1.0×106 BKV copies/μl in patients without HC.The obtained differences were however not statistically significant, due to one individual non-HCpatient with an extremely high BKV copy number. Nevertheless, while 50% of the samples in the HCgroups expressed 1×106 copies/μl or more, only one of the samples in the non-HC group contained avirus quantity higher than 5×105 copies.Conclusions: Although we could not confirm that the C→G mutations in the Sp1 site of BKV wereresponsible for an increased viral load in patients with HC, our data suggest that levels of BKV above104 copies/μl may indicate a risk for HC .
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