The association between polyomavirus BK strains and BKV viruria in liver transplant recipients

Basiratnia

Pediatric Transplantation

et al. 2021

Unusual infections are a well-established adverse consequence of immune suppressant therapy following solid organ transplantation. 1 Leishmaniasis is a protozoal disease that is transmitted by female phlebotomus sandfly bites. [1][2][3][4][5] Depending on the affecting species involved and the host immune system, the infection may manifest as cutaneous, visceral, and mucocutaneous forms. 1,5 Leishmaniasis is a disease of Immune competent children in endemic areas. However, there are growing reports of Leishmaniasis in patients with an immune-suppressive state. 1 Leishmania infection following organ transplantation may occur in four ways: reactivation of latent infection, transmission by an infected graft, blood transfusion, and a new infection. 3 The clinical presentation is also misleading as symptoms, signs, and laboratory data can overlap with other common post-transplant conditions. 3 BK virus (BKV) is a ubiquitous, small DNA virus a member of the polyomavirus family. [6][7][8][9][10] Primary BKV infection occurs during early childhood and is usually asymptomatic. 6,8 The virus remains dormant in the urothelium and will only induce symptoms in

Section: Discussionmentioning

confidence: 99%

Concomitant BK virus infection and visceral Leishmaniasis in a pediatric liver transplant recipient

Basiratnia

Pediatric Transplantation

et al. 2021

“…Despite the fact that 30-50% of all renal recipients develop temporary BK viruria and approximately one-third present viremia, only 1-10% of patients progress to BKVAN [34,35]. Rarely, BKVAN may also appear in native kidneys of other organs recipients -lung, heart, liver and pancreas, as well as bone marrow stem cell [36][37][38][39][40][41][42][43][44]. Symptomatology of BKVN is nonspecific and may vary from asymptomatic infection to elevated serum creatinine.…”

Section: Bk Virus Nephropathymentioning

confidence: 99%

Pathogenicity of BK virus on the urinary system

Krajewski

Kamińska

Poterek

et al. 2020

Cent european J Urol

lence rate among adults. The major sites of BKV appearance are the kidney tubular epithelial cells and urinary bladder surface transitional cells. It usually stays latent, however, BKV replication may become active in various clinical situations of impaired immunocompetence such as solid organ transplantation, bone marrow transplantation, AIDS, pregnancy, multiple sclerosis, administration of chemotherapy or biologic therapy [5]. Nowadays, with the use of potent immunosuppressive agents and enhanced viral surveillance protocols, the BKV has arisen as an important cause of morbidity in renal transplant recipients. BKV is associated with two main complications after transplantation: polyomavirus-associated nephropathy (BKVAN) in 1 to 10% of kidney transplant pa

“…An epidemiologic study demonstrated that approximately 80% of the general population was infected by BKPyV in their childhood [ 14 ]. Following primary infection, BKPyV is persistently hidden in the renourinary tract, and when the immunity of the organ transplant recipients is suppressed, BKPyV rapidly replicates to cause renal inflammation, the occurrence of BKPy-viruria and BKPy-viremia, and sometimes BKPyV-associated nephropathy (BKPyVAN) [ 15 , 16 , 17 , 18 ]. Potent immunosuppressants reduce acute rejection episodes but increase the risk of BKPyVAN and its associated allograft loss.…”

Section: Introductionmentioning

confidence: 99%

High Incidence and Early Onset of Urinary Tract Cancers in Patients with BK Polyomavirus Associated Nephropathy

Chen

et al. 2021

Viruses

Self Cite

Over-immunosuppressed kidney transplant recipients are susceptible to malignancies and BK polyomavirus (BKPyV)-associated nephropathy (BKPyVAN). This study aimed to verify the association between BKPyV infection and urinary tract cancers (UTC). A total of 244 kidney transplant recipients were enrolled at Chang Gung Memorial Hospital from June 2000 to February 2020. Biopsy-proven BKPyVAN patients (n = 17) had worse kidney function (eGFR: 26 ± 13.7 vs. 47.8 ± 31.0 mL/min/1.73 m2). The 5-year allograft survival rates for patients with and without BKPyVAN were 67% and 93%, respectively (p = 0.0002), while the 10-year patient survival was not different between the two groups. BKPyVAN patients had a significantly higher incidence of UTC compared to the non-BKPyVAN group (29.4% vs. 6.6%). Kaplan–Meier analysis showed that the UTC-free survival rate was significantly lower in BKPyVAN patients, and the onset of UTC was significantly shorter in BKPyVAN patients (53.4 vs. 108.9 months). The multivariate logistic regression analysis demonstrated that age (RR = 1.062) and BKVAN (RR = 6.459) were the most significant risk factors for the development of UTC. Our study demonstrates that BKPyVAN patients have greater allograft losses, higher incidence, a lower cancer-free survival rate, and an earlier onset with a higher relative risk of developing UTC compared to non-BKPyVAN patients.