BK Polyomavirus and acute kidney injury in transplant recipients: signaling pathways and molecular mechanisms

Acute kidney injury (AKI) is a condition that can result in changes in both urine production and creatinine levels in the bloodstream, complicating the treatment process and worsening outcomes for many hospitalized patients. BK polyomavirus (BKPyV), a member of the Polyomaviridae family, is prevalent in the population and remains latent in the body. It can reactivate in individuals with a compromised immune system, particularly post-kidney transplant, and can activate various transcription factors and immune mediators. Although reactivation is often asymptomatic, it can present as AKI, which is a risk factor for early loss of the transplanted organ. The immune response to BKPyV is crucial in controlling the virus and safeguarding organs from damage during infection. Understanding BKPyV pathways may offer novel opportunities for effectively treating BKPyV-associated complications. This review seeks to elucidate the potential mechanisms by which BKPyV reactivation can lead to AKI by analyzing various signaling pathways, as well as the identification of molecular mechanisms that BKPyV may utilize to induce AKI.