Polyomavirus BK after Kidney Transplantation – Role of Molecular and Immunologic Markers
نویسندگان
چکیده
Polyomavirus-associated nephropathy in kidney transplantation is viewed as a complication of prolonged, intense immunosuppression, which disrupts the balance between antiviral immune control and polyomavirus replication. The prevalence rate ranges from 1-10% in kidney transplant programs around the world, with graft failure and return to dialysis in > 50%. Most cases are caused by the human polyomavirus BK, which asymptomatically infects more than 80% of the general population. Reactivation of BK virus replication and high urine viral loads precede increasing plasma BK viral loads and histologically defined as well as clinically manifest nephropathy. Quantitative real-time polymerase chain reaction protocols have proven valuable as surrogate markers to follow the course of polyomavirus-associated nephropathy and to guide preemptive reduction of immunosuppression. As these assays enter clinical routine diagnostic laboratories, quality control becomes important. Testing of BK virus-specific antibodies and T-cells is currently being explored for a better characterization of the virus/host balance. The BK virus-like particles IgG in enzyme-linked immunosorbent essays are recognized as sensitive indicators of recent BK virus exposure. However, no humoral immune responses have been identified to correlate with protection from BKV viremia or disease. BK virus-specific T-cells are generally of low frequencies in the peripheral blood of both healthy donors and kidney transplant patients alike, but significantly increase at the time when plasma BK virus loads decrease, hence representing relatively late indicators of regaining control. We discuss the currently available data on molecular and immune markers regarding promises and caveats. (Trends in Transplant. 2009;3:85-102) Corresponding author: Hans H. Hirsch, [email protected]
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