异基因造血干细胞移植中巨细胞病毒潜伏感染的防治

目的:观察依据异基因造血干细胞移植前受者巨细胞病毒(CMV)血清学检测结果采取不同的CMV感染防治方案的临床效果。方法:行异基因造血干细胞移植的37例患者,移植预处理前1周依据受者CMV血清学检测结果,对于移植前PP65抗原、CMV抗体及CMV-DNA定量均阴性的受者,应用阿昔洛韦预防CMV感染;移植前PP65、IgM抗体及DNA定量阴性,IgG抗体阳性的受者应用静脉更昔洛韦预防CMV感染。预处理中及移植后均采用阿昔洛韦进行病毒感染的预防,并定期检测PP65及CMV-IgM和CMV-DNA定量,当出现PP65阳性和/或CMV-IgM阳性、病毒复制增加时,给予更昔洛韦或膦甲酸钠联合人免疫球蛋白治疗。结果:36例受者移植后检测CMV抗体IgG均为阳性,巨细胞病毒血症占18.9%(7/37),CMV病占10.8%(4/37),CMV感染的时间为移植后+27～+65d,CMV感染多见于非血缘、HLA不全相合及发生aGVHD的患者,经更昔洛韦和或膦甲酸钠治疗后无一例因CMV病死亡。应用不同预防CMV感染方法的患者间造血重建时间无明显差异。结论:依据受移植前受者血清学检测结果给予不同的预防方案并结合预先治疗方案防治CMV感染可以明显减少CMV潜伏感染转变为CMV病的概率,且对造血重建无影响。     

抢先抗巨细胞病毒治疗策略在不同类型造血干细胞移植中的疗效比较

目的 对不同类型异基因造血干细胞移植(HSCT)的巨细胞病毒(CMV)感染患者采用统一的抢先治疗指征,比较抗病毒治疗的效果,从而评价抢先治疗策略的临床应用价值.方法 进行异基因HSCT患者318例,自移植后采用实时定量(RQ)-PCR法监测血浆CMV-DNA水平,其中136例出现CMV感染,全相合HSCT 31例,亲缘半相合HSCT 88例,非血缘HSCT 17例.三种类型移植采用相同的抗病毒抢先治疗指征,比较CMV-DNA拷贝数的转阴率、CMV病的发生率及患者的长期生存率.结果 136例CMV感染患者分别采用更昔洛韦、膦甲酸钠或缬更昔洛韦进行抗病毒抢先治疗,全相合、半相合及非血缘移植组治疗的中位时间相近,三组患者CMV-DNA最终转阴率相似(96.8%,93.2%,88.2%),组间比较差异均无统计学意义(P>0.05).抢先治疗后三组患者发生CMV肺炎及肠炎的比例及死于CMV病几率的差异也无统计学意义(P>0.05).各类型移植患者的长期生存率差异无统计学意义(P=0.88),发生Ⅱ～Ⅳ度急性移植物抗宿主病(aGVHD)患者生存率明显低于0～Ⅰ度aGVHD患者(P=0.036).结论 不同类型造血干细胞移植术后的CMV感染患者,采用基于RQ-PCR监测的抢先治疗策略可达到相同的疗效.     

异基因造血干细胞移植后巨细胞病毒感染的预先治疗

目的:探讨预防治疗及预先治疗对异基因造血干细胞移植后CMV感染的干预作用.方法:225例异基因造血干细胞移植患者中160例接受预先治疗,65例接受预防治疗,用logistic回归模型分析影响CMV感染的危险因素.结果:预先治疗组与预防治疗组比较,CMVpp65抗原血症、CMV病和CMV病死亡率分别为28.1%(35.3%,P>0.05),1.9%(12.3%,P<0.05)和0.6%(10.7%,P<0.01).单倍体相合移植组出现CM-Vpp65血症33.0%(40.0%,P>0.05)、CMV病发生率1.9%(12.0%,P<0.05)、死亡率0.0%(10.0%,P<0.05),均低于相合移植.单倍体相合移植组中CMVpp65阳性发生的主要危险因素为重症GVHD、移植前给予抗CMV治疗以及是否混合其他严重感染.结论:异基因移植后预先治疗优于预防治疗,可以明显减低CMV病的发生和死亡.     

中国造血干细胞移植后巨细胞病毒感染管理的现状与进展

巨细胞病毒(CMV)感染是造血干细胞移植(HSCT)后常见的合并症之一, 可造成诸多直接或间接的不良后果, 严重影响移植疗效。近年来, 随着新的检测技术和抗病毒药物的出现, 中国在CMV感染的诊断、预防及治疗中均取得了较多进展。传统抗病毒药物能减少早期CMV疾病发生率, 但存在较强的毒性, 而免疫细胞, 尤其是细胞毒性T淋巴细胞对控制CMV活化起重要作用。因此, 过继免疫疗法成为CMV感染防治的新思路。本文就异基因HSCT后CMV感染的流行病学、危险因素、诊断监测、预防治疗、免疫探索以及过继免疫疗法进行中国经验的总结, 以期为临床工作提供参考。     

乙型肝炎病毒感染患者进行异基因造血干细胞移植的安全性评价

目的:对伴有乙型肝炎病毒(HBV)感染的恶性血液病患者抗病毒治疗后进行异基因造血干细胞移植(allo- HSCT)的安全性进行评价.方法:allo- HSCT患者45例,均为HBV感染的恶性血液病患者,移植前感染HBV的患者和供者均给予拉米夫定和(或)阿德福韦/恩替卡韦抗病毒治疗;移植前对HBV-DNA的拷贝数进行评估...     

非清髓造血干细胞移植治疗再生障碍性贫血

目的:探讨非清髓性造血干细胞移植(NST)治疗再生障碍性贫血(再障)的方法及疗效。方法:采用非清髓预处理方案进行造血干细胞移植治疗再生障碍性贫血2例。1例为同胞间HLA配型6个位点完全相合的异基因外周血造血干细胞移植,另1例为同胞间HLA配型6个位点完全相合的脐血移植。预处理方案主要由抗胸腺细胞球蛋白(ATG)和环磷酰胺组成。用环孢素A和霉酚酸酯(MMF)预防移植物抗宿主病(GVHD)。结果:2例患者均获造血重建(分别为 5及 9d),2例均未发生GVHD。1例患者在治疗期间未出现感染表现,另1例患者出现CMV感染,给予更昔洛韦病情得以完全控制。2例分别无病生存8及17个月。结论:非清髓造血干细胞移植简便安全,并发症少,疗效好,为治疗再生障碍性贫血有效方法。     

改良非清髓性异基因造血干细胞移植治疗SAA疗效观察

目的探讨非清髓性异基因造血干细胞移植(NAST)治疗重型再生障碍性贫血(SAA)的方法及疗效。方法对20例急性SAA患者进行NAST,预处理采用小剂量环磷酰胺、抗淋巴细胞球蛋白或抗胸腺细胞球蛋白;移植后采用环孢菌素、骁悉、抗CD25预防移植物抗宿主病(GVHD)。采用短串联重复序列复合扩增技术检测供者植入情况。结果10例异基因外周血造血干细胞移植患者造血功能获得快速重建;8例脐血造血干细胞移植患者均未植入,但自身造血亦获得安全重建。发生急性GVHD1例,慢性GVHD2例,严重感染性休克、间质性肺炎、败血症各1例均治愈,突发心衰死亡1例,造血重建失败并发感染死亡2例。结论改良NAST疗效肯定、植入率高、并发症少、造血功能恢复快,是治疗SAA的有效方法。     

异基因造血干细胞移植后巨细胞病毒感染的发病情况及疗效分析

目的：探讨异基因造血干细胞移植（allo-HSCT）后,巨细胞病毒（CMV）感染的发病情况及抗病毒治疗的疗效。方法：对在我所接受allo-HSCT的患者23例进行回顾性分析,均应用荧光定量PCR法（FQ-PCR法）检测外周血CMV-DNA含量。CMV感染应用更昔洛韦（GCV）10mg.kg-1.d-1进行治疗。结果：23例患者中7例移植后发生CMV感染,占30.43%。GCV治疗的总有效率约为85.71%。6例在GCV治疗过程中出现白细胞和血小板减少。结论：FQ-PCR法可以应用于allo-HSCT后早期准确诊断CMV感染。GCV对allo-HSCT后CMV感染的预防及治疗效果可靠。     

Notch信号通路在急性移植物抗宿主病中的作用

目的:分析异基因造血干细胞移植后患者Notch1的表达,了解Notch1信号通路与急性移植物抗宿主病发生、发展的关系。方法:采集54例异基因造血干细胞移植后患者外周血,同期采集26例自体造血干细胞移植患者和10例正常志愿者外周血标本作为对照,检测Notch1和Hes-1 mRNA的表达,分析其与急性移植物抗宿主病的关系。结果:异基因造血干细胞移植患者Notch1和Hes-1 mRNA表达较自体造血干细胞移植患者和正常志愿者高(P0.05),其中急性移植物抗宿主病患者Notch1 mRNA表达明显高于非急性移植物抗宿主病患者、自体造血干细胞移植患者及正常志愿者(P0.05)。Notch1 mRNA的表达与急性移植物抗宿主病总体分度呈正相关,急性移植物抗宿主病越严重,Notch1 mRNA的表达越高(P0.05)。结论:Notch1信号参与调节急性移植物抗宿主病;Notch1及其靶基因的表达与急性移植物抗宿主病的严重程度密切相关。     

短串联重复序列多态性检测非清髓造血干细胞移植造血嵌合体的研究

近来 ,随着非清髓异基因造血干细胞移植 (NST)的开展 ,造血嵌合体的研究已成为异基因造血干细胞移植 (Allo SCT)的热点课题。我们利用短串联重复序列 (STRs)的高度多态性和竞争性 (STR PCR)的高度敏感性建立了相对定量检测移植后造血嵌合体的技术方法 ,并对 2 7例HLA相合的NST患者的造血嵌合体进行动态的前瞻性研究 ,探讨嵌合与移植排斥的关系。一、资料和方法1 供受者 :2 0 0 0年 3月至 2 0 0 1年 12月共对 2 7例NST患者进行嵌合体检测。其中我院 2 1例 ,沈阳第 2 0 1医院 6例 ;男 18例 ,女 9例 ,年龄 2 1～ 5 9岁 ,中位年龄 36…     

CMV disease in AIDS patients: incidence of CMV disease and relation to survival in a population-based study from Oslo

CMV disease is an important cause of morbidity and mortality in patients with AIDS. The purpose of this study was to investigate the incidence of CMV disease in a well-defined population of AIDS patients with a high rate of autopsy. No such study has previously been published from Scandinavia. A total of 248 patients who developed clinical AIDS in Oslo during the period 1 January, 1983 to 31 December, 1995 were included. Autopsy was performed in 152 of 213 deaths (71.3%). CMV disease was diagnosed in 95 patients. In the autopsy group, 73 patients (48%) had CMV disease, and in 52 of these patients CMV disease was first detected at autopsy. Retinitis was the most frequent manifestation, followed by adrenalitis, pneumonitis, encephalitis and gastrointestinal disease. No intravenous drug users (IVDUs) were diagnosed alive with CMV disease. All patients diagnosed with CMV disease before death had evidence of CMV disease at autopsy despite anti-CMV treatment. CMV disease was associated with increased risk of death. We conclude that CMV disease was frequent in patients with AIDS during the study period, was associated with increased mortality and was often diagnosed too late for the administration of appropriate therapy.     

Clinico-pathological study of cytomegalovirus (CMV) in AIDS autopsies: under-recognition of CMV pneumonitis and CMV adrenalitis

Abstract Background: Cytomegalovirus (CMV) is a common cause of morbidity in human immunodeficiency virus (HIV) infected patients, predominantly when severe immunosuppression has occurred. Although CMV infection of the retina and gastrointestinal tract is well recognised as causing substantial morbidity, the significance of infection at other sites, in particular the lungs and adrenal glands is unclear. Aims: To assess the extent of CMV infection in postmortem examinations performed on HIV-infected patients. To estimate the degree of concordance between clinical and postmortem findings and the effect of prior diagnosis and/or treatment of CMV infection. Methods: The postmortem examination findings and clinical records of 25 consecutive HIV-infected patients who underwent a complete autopsy were examined. Results: CMV infection was demonstrated in 19 patients (76%) at postmortem examination, with the most common sites of infection being the adrenal glands (56%) and lungs (44%). Concordance between clinical diagnosis of CMV infection and postmortem findings was low with only five of 19 patients (26%) having an antemortem diagnosis. No patient with CMV infection of the lungs or adrenal glands had a clinical diagnosis made, despite four patients having florid CMV pneumonitis at postmortem examination; in three the probable cause of death. Conclusion: CMV infection is a common postmortem finding in HIV-infected patients but the concordance between clinical diagnosis and autopsy findings is low. CMV appears to be a significant pathogen in HIV-related respiratory disease. (Aust NZ J Med 1995; 25: 503–506.)     

Treatment of CMV retinitis with intravitral ganciclovir in the HAART era

OBJECTIVE: To describe the course and outcome of cytomegalovirus (CMV) retinitis among AIDS patients treated with intravitreal ganciclovir and systemic highly active antiretroviral therapy (HAART). The secondary objective was to compare the course of CMV retinitis between patients receiving HAART and those not receiving this treatment. DESIGN: A retrospective cohort design consisting of 21 eyes from 16 patients with AIDS and CMV retinitis consecutively enrolled between January 1996 and August 1999. All patients received intravitreal ganciclovir therapy, and half of the patients began HAART as well. Duration of intravitreal therapy and ensuing disease quiescence, as well as CD4+ T cell counts at diagnosis and at cessation of ganciclovir, were calculated. Secondly, instantaneous hazards for outcomes such as CMV retinitis progression, ocular complications and mortality were compared. SETTING: Tertiary care centre in Ottawa, Ontario. RESULTS: Five of eight patients receiving HAART discontinued intravitreal ganciclovir after a mean treatment period of 428 days. During this period, their mean CD4+ count rose from 7.5 to 190microL. Subsequently, none of these patients experienced retinitis progression during follow-up periods lasting up to 820 days (mean of 617 days). Progression of CMV retinitis was 11.4 times more likely among those not receiving HAART (P=0.049). CONCLUSIONS: On initiating HAART, patients with CMV retinitis may enjoy significant recovery in CD4+ counts and sustained retinitis quiescence without specific anti-CMV therapy. Intravitreal ganciclovir injections seem well suited to offer effective CMV control during temporary periods of decreased CD4+ counts while awaiting HAART-mediated immune system reconstitution.     

Cytomegalovirus (CMV) blood DNA load, CMV retinitis progression, and occurrence of resistant CMV in patients with CMV retinitis

BACKGROUND. The amount of cytomegalovirus (CMV) DNA in the blood (CMV load) may be a marker for detection of resistant CMV.METHODS. A total of 165 patients with AIDS and CMV retinitis had CMV load measurements (plasma and leukocyte) and cultures performed every 3 months; these measurements were correlated with CMV resistance to antiviral drugs and CMV retinitis progression (from masked readings of retinal photographs).RESULTS. Detectable plasma and leukocyte CMV loads were associated with CMV retinitis progression (odds ratios [OR], 6.3; P<.0001 and OR, 6.6; P<.0001, respectively), phenotypic resistance (OR, 6.1; P<.0001 and OR, 23.4; P=.0002, respectively), and genotypic resistance (OR, 17.5; P<.0001 and OR, 51.6; P=.0004, respectively). The sensitivity, specificity, and positive and negative predictive values of plasma CMV loads were 0.47, 0.86, 0.36, and 0.91, respectively, for progression and 0.59, 0.81, 0.07, and 0.99, respectively, for resistance; those of leukocyte CMV loads were 0.52, 0.83, 0.35, and 0.91, respectively, for progression and 0.82, 0.78, 0.08, and 0.99, respectively, for resistance. A detectable plasma CMV load at the time of diagnosis of CMV retinitis was associated with mortality (median survival time, 13.6 vs. 29.7 months; P=.007).CONCLUSIONS. CMV load has limited clinical utility, because of its low positive predictive value. Its high negative predictive value for occurrence of resistant CMV suggests that it may have utility as a screening tool to exclude resistance.     

Investigation of Cytomegalovirus in Intestinal Tissue in a Country With High CMV Seroprevalence

Background: In Turkey, cytomegalovirus (CMV) seropositivity has been reported to be high, between 85 and 100%. CMV has been responsible for disease exacerbation in inflammatory bowel disease (IBD). We aimed to evaluate the presence of CMV in intestinal tissue by immunohistochemical staining in IBD and non-IBD patient groups, in a country with high CMV seroprevalence.Methods: In this prospective cross-sectional study, the presence of intestinal CMV was investigated with tissue immunohistochemistry (IHC) staining, which is accepted as the gold standard method, and with polymerase chain reaction (PCR) in tissue and blood. Patients (≥18 years old, n = 189) who had a colonoscopic biopsy between January and May 2017 were included in the study at our hospital. Clinical, laboratory, endoscopic, and histopathological data of patients were assessed by dividing them into IBD (n = 34) and non-IBD (n = 155) groups.Results: In this study, 567 colonic biopsy samples from 189 patients were evaluated. Tissue IHC staining was positive for 3 (1.58%) non-IBD patients. One of them was diagnosed as CMV ileitis. CMV DNA was also detected in 14 plasma (7.40%, <80-469 copies/mL) and 20 tissue samples (10.69%, 7-15 289 copies/mL). Tissue IHC staining is accepted as the gold standard for CMV ileitis, and the sensitivity and specificity of tissue PCR was 33% and 89.67%, while the sensitivity and specificity of plasma PCR was 66.66% and 93.54%, respectively.Conclusion: Although CMV seroprevalence is high in Turkey, CMV ileitis was diagnosed in only one non-IBD patient (0.53%). Compared to tissue IHC staining, the sensitivity of tissue and blood CMV PCR was low while their specificity was higher.     

造血干细胞移植后巨细胞病毒感染患者糖蛋白B基因分型的初步研究

目的初步探讨造血干细胞移植(HSCT)后巨细胞病毒(CMV)感染患者CMV糖蛋白(G)B基因分型及其与致病性的关系。方法研究了2001年3月至2003年12月在我院行HSCT的患者38例,均采用巢式PCR方法检测CMV GBDNA为阳性,对PCR产物用RsaⅠ和HinfⅠ内切酶进行了酶切分型。结果Ⅰ型19/38例(50.0%),Ⅱ型3/38例(7.9%),Ⅲ型14/38例(36.8%),Ⅰ与Ⅲ混合型2例。Ⅰ型感染预后良好,Ⅲ型与致死性间质性肺炎(IP)发生有明显的相关性。Ⅰ、Ⅲ型患者移植物抗宿主病(GVHD)的发生率差异无统计学意义。结论CMVGB蛋白的基因分型与CMV的IP发生有关,与GVHD的发生无明显相关性。     

常频机械通气和鼻塞式持续气道正压通气在新生儿呼吸衰竭的疗效对比

目的比较常频机械通气(CMV)与鼻塞式持续气道正压通气(NCPAP)治疗新生儿呼吸衰竭的临床疗效及并发症情况。方法回顾性分析2012年1月至2014年12月该院新生儿科收治的125例呼吸衰竭并应用NCPAP及CMV治疗的新生患儿,比较治疗后两组患儿的治疗效果、血气分析、生命体征及并发症情况。结果 NCPAP组有效率为84.5%,CMV组有效率为79.6%,两组之间比较差异无统计学意义(P0.05)。通气治疗后两组患儿血气分析、生命体征均逐渐恢复正常并维持平稳,各项指标均得到明显改善。NCPAP组治疗过程中出现的并发症发生率为8.5%%,明显低于CMV组并发症的发生率(31.5%)(P0.05)。结论 NCPAP治疗新生儿呼吸衰竭疗效与常频机械通气差异不大,但具有无创、操作简易的优势,是临床治疗新生儿呼吸衰竭的一种较为理想通气模式。     

Cytomegalovirus (CMV)-encoded UL144 (truncated tumor necrosis factor receptor) and outcome of congenital CMV infection

BACKGROUND: Cytomegalovirus (CMV) is the most common congenital infection in humans. The effect of viral strains on the outcome of congenital CMV is debated. We evaluated whether UL144 polymorphisms in amniotic fluid from CMV-infected Italian women were associated with terminations of pregnancy, subsequent disease in their offspring, or viral load. METHODS: The study was nested within a prenatal CMV program. We sequenced the UL144 gene from 66 amniotic-fluid samples, without knowledge of pregnancy outcome. We performed data analyses on 56 samples for which all information was available. RESULTS: Genotype C was associated with termination of pregnancy (P=.03). Genotype B was associated with fewer terminations of pregnancy (P=.003). A possible association was found between genotype C and symptomatic disease in newborns (odds ratio, 8.81 [95% confidence interval, 0.48-164.02]; P=.05). There was no association between specific genotype and the viral load in amniotic fluid. Symptomatic newborns who had the most common UL144 genotype (B) were more likely to have higher viral loads than were asymptomatic infants (P=.003). CONCLUSIONS: UL144 polymorphisms may be associated with the outcome of congenital CMV infection. Larger studies should be conducted to confirm this association, before genotype analysis can be used, along with other factors, in considering terminations of pregnancy.     

Pre‐transplant cytomegalovirus (CMV) serostatus remains the most important determinant of CMV reactivation after allogeneic hematopoietic stem cell transplantation in the era of surveillance and preemptive therapy

B. George, N. Pati, N. Gilroy, M. Ratnamohan, G. Huang, I. Kerridge, M. Hertzberg, D. Gottlieb, K. Bradstock. Pre‐transplant cytomegalovirus (CMV) serostatus remains the most important determinant of CMV reactivation after allogeneic hematopoietic stem cell transplantation in the era of surveillance and preemptive therapy.
Transpl Infect Dis 2010: 12: 322–329. All rights reserved Abstract: Between January 2001 and June 2008, 315 adult patients (median age 43 years, range 16–65) including 203 males and 112 females undergoing hematopoietic stem cell transplantation (HSCT) had serial monitoring for cytomegalovirus (CMV) followed by initiation of preemptive therapy. The majority (62.1%) had a conventional myeloablative transplant with 116 (36.9%) having a reduced‐intensity conditioning (RIC) transplant, using either matched sibling/family (63.3%) or unrelated donors (36.7%). Graft source was peripheral blood stem cells in 257 (81.5%), bone marrow in 41 (13.1%), and cord blood in 16 (5.4%). T‐cell depletion with anti‐thymocyte globulin or alemtuzumab was used in 35%. Based upon CMV serostatus, patients were classified into low risk (donor [D]?/recipient [R]?), intermediate risk (D+/R?), or high risk (D?/R+ or D+/R+). Serial weekly monitoring for CMV viremia was performed using a qualitative polymerase chain reaction (PCR) and when positive, quantification was done using either pp65 antigen or a quantitative PCR. CMV reactivation was seen in 123 patients (39.1%) at a median of 50 days post HSCT (range 22–1978). CMV serostatus was the most important risk factor with incidence of 53% in the high‐risk group (53.3%) compared with 10.2% in the intermediate risk and 0% in the low‐risk group (P<0.0001). Other significant risk factors identified included use of alemtuzumab during conditioning (P=0.03), RIC transplants (P=0.06), and the presence of acute graft‐versus‐host disease (GVHD) (P<0.0001). On a multivariate analysis, CMV serostatus, RIC transplants, and acute GVHD remained independent predictors of CMV reactivation. All were treated with antiviral therapy with responses seen in 109 (88.6%). Sixteen patients (13%) developed CMV disease at a median of 59 days post HSCT (range 26 days–46 months), 8 of whom died. At a median follow up of 43 months (range 6–93), 166 patients (52.6%) are alive with a significantly higher survival among patients without CMV reactivation (57.2%) as compared with patients with CMV reactivation (45.5%; P=0.049). CMV reactivation and disease remains a major problem in high‐risk patients undergoing allogeneic HSCT. Novel prophylactic measures such as immunotherapy and drug prophylaxis need to be considered in this specific group of patients.     

Cytomegalovirus (CMV) glycoprotein B genotypes and response to antiviral therapy,in solid-organ-transplant recipients with CMV disease

Cytomegalovirus (CMV) can be classified into 4 glycoprotein B (gB) genotypes, on the basis of sequence variation in the UL55 gene. We assessed the effect that CMV gB genotype has on virologic and clinical response to therapy, in 50 solid-organ-transplant recipients with CMV disease. CMV loads were determined at regular intervals after the start of therapy. Genotype results were correlated with CMV-load kinetics in response to therapy with ganciclovir. At the onset of treatment, the distribution of CMV gB genotypes was as follows: gB1, 19/50 (38%); gB2, 9/50 (18%); gB3, 12/50 (24%); gB4, 2/50 (4%); and mixed-genotype infection, 8/50 (16%). Between viral genotype groups, time to clearance of CMV, failure to clear CMV, and calculated CMV-load half-life after the start of therapy were not significantly different. The CMV gB genotype did not affect the rate of disease recurrence or occurrence of tissue-invasive disease. It appears that the gB genotype, which causes CMV disease, does not significantly influence CMV-load kinetics or clinical response to therapy.