| BackgroundPolyomaviruses were designated as one of the subfamilies of the family Papovaviridae. The polyomavirus family includes two human pathogens, JC virus(JCV) and BK virus (BKV).The genome of BKV is a closed circular,double-stranded molecule of DNA approximately 5kb in size. It consists of the genetically conserved coding region and the hypervariable noncoding regulatory region(NCRR). The coding region is functionally divided between the early and late gene coding regions.The early genes that encode the large T antigen and small t antigen are expressed soon after infection of the host cell. The late genes, consisting of the structural proteins VP1, VP2, VP3 and the agnoprotein genes, and predominately expressed after genomic replication has been initiated.Almost everyone is exposed to BKV as a child,The primary infection is either completely asymptomatic or takes the form of a mild respiratory illness. The virus then enters a latent state and resides primarily in the kidney. In 0.5% to 20% of immune-competent hosts, polyomaviruses can be periodically reactivated and reenter into a replicative cycle.Disease caused by polyomaviruses is seen only in immune-compromised hosts. Depending on the viral strain and the type of the underlying suppression of the immunesystem, different illnesses prevail. In the setting of kidney transplantations, the prevalence of latent infections with polyomaviruses is high. Thus , latent polyomaviruses are likely often passed in the graft from the donor to the host. Asymptomatic reactivation polyomavirusese is also commonly seen in the healthy kidney transplant recipients(10%-60%). Such activation normally lasts for only a short duration and renal allograft function remains unaltered. Following reactivation, if a high level of replication continues, lysis of tubular cells releases BKV into tubules with bare basement membrane. It is thought that this results in leakage of virus particles into the medullary interstitium, from where the virus gains access to the blood. Viremia signifies a state of extremely high virus activity, with imminent danger of end organ damage. If allowed to proceed unchecked, this results in virus DNA replication in target cells, target cell destruction, and precipitation of BKV disease.(ie:BKVAN -- BK virus-associted nephropathy)BKVAN, that is , the clinical syndrome of significant BKV infection of the renal allograft, occurs infrequently. The reported prevalence ranges from 1% to8%. It is most common in the first year after transplantation, when immunosuppression is most intense.BKVAN is usually associated with ureteral obstruction,lymphoceles,bacterial urinary tract infection, hematuria, and systemic CMV infection. BKVAN mimicks rejection or drug toxicity, confusion between these complications may lead to either anti-rejection therapy,with the risk of over-immunosuppression or reduction of immosuppression, with the risk of graft loss.To make a diagosis of BKVAN, histologic examination with immunohistochemistry is essential. The hallmark of BKVAN on light microscopic examination is an interstitial nephritis largely composed of a mononuclear lymphocytes, tubulitis , and atypical enlarged tubular nuclei with viral inclusion. Detection of BKV by plasma PCR has a potential both to diagnose the BKVAN and to follow the clinicalinfection. Screening for detection of BKV in the urine is a simple test. The treatmemt for BKVAN remains careful adjustment of immunosuppression, and new antiviral approaches are currently being evaluated.There is no report about BKV infection and BKV -induced diseases after kidney transplantation in China. In this paper, we detected BKV DNA in the urine of renal allograft recipients using PCR method combined with DNA sequencing. The purpose of the present study was to select a sensitive ,specific method so as to guide the diagnosis and treatment of the BKV induced diseases after kidney transplantation. MethodsWe investigated three groups at the kidney diseases center of the 1st affiliated hospital of zhejiang u... |
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