Our data indicate that the risk of developing an OI for a person receiving potent antiretroviral therapy is highest during the initial months of therapy. Baseline CD4 cell count and immunologic and virologic response to treatment were strong predictors of disease progression in patients receiving potent therapy. Individuals with CD4 cell counts of 50 x 10(6)/L or below may need close clinical surveillance after initiation of potent therapy.

No consensus exists on whether acyclovir prophylaxis should be given for varicella-zoster virus (VZV) prophylaxis after hematopoietic cell transplantation because of the concern of "rebound" VZV disease after discontinuation of prophylaxis. To determine whether rebound VZV disease is an important clinical problem and whether prolonging prophylaxis beyond 1 year is beneficial, we examined 3 sequential cohorts receiving acyclovir from day of transplantation until engraftment for prevention of herpes simplex virus reactivation (n ‫؍‬ 932); acyclovir or valacyclovir 1 year (n ‫؍‬ 1117); or acyclovir/valacyclovir for at least 1 year or longer if patients remained on immunosuppressive drugs (n ‫؍‬ 586). In multivariable statistical models, prophylaxis given for 1 year significantly reduced VZV disease (P < .001) without evidence of rebound VZV disease. Continuation of prophylaxis beyond 1 year in allogeneic recipients who remained on immunosuppressive drugs led to a further reduction in VZV disease (P ‫؍‬ .01) but VZV disease developed in 6.1% during the second year while receiving this strategy. In conclusion, acyclovir/valacyclovir prophylaxis given for 1 year led to a persistent benefit after drug discontinuation and no evidence of a rebound effect. To effectively prevent VZV disease in long-term hematopoietic cell transplantation survivors, additional approaches such as vaccination will probably be required. (Blood. 2007; 110:3071-3077)

We conducted a 12-year retrospective study to determine the effects that the community respiratory-virus species and the localization of respiratory-tract virus infection have on severe airflow decline, a serious and fatal complication occurring after hematopoietic cell transplantation (HCT). Of 132 HCT recipients with respiratory-tract virus infection during the initial 100 days after HCT, 50 (38%) developed airflow decline < or =1 year after HCT. Lower-respiratory-tract infection with parainfluenza (odds ratio [OR], 17.9 [95% confidence interval {CI}, 2.0-160]; P=.01) and respiratory syncytial virus (OR, 3.6 [95% CI, 1.0-13]; P=.05) independently increased the risk of development of airflow decline < or =1 year after HCT. The airflow decline was immediately detectable after infection and was strongest for lower-respiratory-tract infection with parainfluenza virus; it stabilized during the months after the respiratory-tract virus infection, but, at < or =1 year after HCT, the initial lung function was not restored. Thus, community respiratory virus-associated airflow decline seems to be specific to viral species and infection localization.

We performed a case-control study to determine the association of BK plasma viremia with hemorrhagic cystitis (HC) in hematopoietic cell transplant (HCT) recipients. Thirty cases of HC (14 of which occurred after platelet engraftment with documented BK viruria [BK-HC]) were compared with matched controls. Weekly plasma samples were tested for BK virus DNA by polymerase chain reaction (PCR). BK viremia detected before or during the disease was independently associated with HC (adjusted odds ratio ‫؍‬ 30, P < .001); BK viremia was even important before clinical symptoms of HC occurred (odds ratio ‫؍‬ 11, P < .001). Cases of HC and BK-HC had a significantly higher peak of BK plasma viral load than controls. IntroductionIn hematopoietic cell transplant (HCT) recipients, hemorrhagic cystitis (HC) occurring after engraftment has been correlated with presence of BK virus in urine, 1,2 and high viral load of BK virus in urine has been associated with a higher risk of BK-associated HC. 3 However, viruria is common even in asymptomatic immunocompromised patients, making a direct causative role of BK virus difficult to establish. 4 Presence of viral DNA in plasma of latent viruses such as cytomegalovirus (CMV), adenovirus, and EpsteinBarr virus has been shown to be a reliable marker of clinical disease in different transplant settings. 5,6 While BK viremia is a sensitive and specific indicator of BK nephritis in solid organ transplants, 7 BK viremia has been reported to occur in asymptomatic HCT recipients. 8 We conducted a matched case-control study to assess whether plasma BK DNA viral load was associated with HC following hematopoietic cell transplantation. Study designAll patients who underwent their first allogeneic hematopoietic cell transplantation at the Fred Hutchinson Cancer Research Center (FHCRC) from January 1979 to October 2003 and who had frozen plasma samples available for retrospective testing of BK virus DNA were included in the study. The study received institutional review board approval at FHCRC. Each patient included in the study had previously signed an informed consent form allowing the storage and the use of their blood products for future research. We identified patients with grade 2 to 4 HC from the FHCRC database, reviewed their medical records, and collected the clinical data relevant to hematuria. HC was divided into 4 categories according to the severity of hematuria. 4 Patients were required to have at least one sample within 3 weeks before and one week after onset of HC. Each patient except one had plasma samples available before HC. There were 6 patients who had samples available only during HC. At least 2 controls per patient, matched by age (exact) and decade of transplantation, were used. The matched controls had available samples drawn during the corresponding time interval. Patients with HC who underwent a bladder biopsy were retrospectively tested for BK virus by in situ hybridization (ISH). The laboratory records of cases were reviewed for presence of adenovirus (culture or direct ...