Abstract
BK polyomavirus (BKV) mainly causes infection in uroepithelial and renal tubular epithelial cells of either immunocompetent or immunocompromised hosts. Despite asymptomatic or mild clinical features in immunocompetent hosts with BK infection, serious complications are frequently found in immunocompromised patients, especially patients with kidney transplantation. Accordingly, BKV-associated nephropathy (BKVN) demonstrates a wide range of clinical manifestations, including ureteric stenosis and hemorrhagic cystitis. In addition, BKV re-infection in post-kidney transplantation is also a main cause of kidney allograft dysfunction and graft loss. Since the direct anti-BKV is unavailable, immune response against BKV infection is the main mechanism for organism control and might be a novel strategy to treat or suppress BKV. As such, the innate immunity, consisting of immune cells and soluble molecules, does not only suppress BKV but also enhances the subsequent adaptive immunity to eradicate the virus. Furthermore, the re-activation of BKV in BKVN of kidney-transplanted recipients seems to be related to the status of innate immunity. Therefore, this review aims to collate the most recent knowledge of innate immune response against BKV and the association between the innate immunity status of kidney-transplanted recipients and BKV re-activation.
Highlights
BK polyomavirus (BKV) is a double-stranded DNA virus in Polyomaviridae family that is originally described in 1971 from a patient with kidney transplantation [1]
Macrophages coupled with dendritic cells (DCs) stimulate the tion, whereas natural killer (NK) cells are mainly involved in antibody-dependent cellular cytotoxicity innate immunity response through major histocompatibility complexes (MHCs)
Α-defensins are composed of human neutrophil peptides (HNP) 1–4, which are expressed in human α-defensin 5 (HD5)–6 immune cells that are found in the small intestine and HD5 cells that are found in the urogenital tract [48]
Summary
BK polyomavirus (BKV) is a double-stranded DNA virus in Polyomaviridae family that is originally described in 1971 from a patient with kidney transplantation [1]. In kidney-transplanted recipients, BKV is associated with a wide range of clinical presentations, including viruria, viremia, ureteric stenosis, and hemorrhagic cystitis [3]. Transplantology 2022, 3 the most common manifestation of BKV-associated complications in hematopoietic stem cell transplant (HSCT) recipients is hemorrhagic cystitis [5]. The soluble molecules are a complement, ficolins and lectins [10], transferrin and lactoferrin [11] It seems that innate immunity may be a key parameter against BKV and BKVN pathogenesis. This review aims to describe recent knowledge of the cellular and molecular immunobiology that is involved in the host immune system against BKV, the innate immune response and the innate immunity in kidney-transplanted recipients with BKVN
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