Amandeep Kaur1, Maud Wilhelm1, Sabrina Wilk1, Hans H Hirsch1,2,3. 1. Department Biomedicine, Transplantation and Clinical Virology, University of Basel. 2. Clinical Virology, Laboratory Medicine. 3. Infectious Diseases and Hospital Epidemiology, University Hospital Basel, Basel, Switzerland.
Abstract
PURPOSE OF REVIEW: BK polyomavirus (BKPyV) has emerged as a significant cause of premature graft failure after kidney transplantation. Without effective antiviral drugs, treatment is based on reducing immunosuppression to regain immune control over BKPyV replication. The paradigm of high-level viruria/decoy cells, BKPyV-DNAemia, and proven nephropathy permits early interventions. Here, we review recent findings about BKPyV-specific antibody and T-cell responses and their potential role in risk stratification, immune monitoring, and therapy. RECENT FINDING: Kidney transplant recipients having low or undetectable BKPyV-specific IgG immunoglobulin G (IgG) are higher risk for developing BKPyV-DNAemia if the donor has high BKPyV-specific IgG. This observation has been extended to neutralizing antibodies. Immunosuppression, impaired activation, proliferation, and exhaustion of BKPyV-specific T cells may increase the risk of developing BKPyV-DNAemia and nephropathy. Clearance of BKPyV-DNAemia was correlated with high CD8 T cell responses to human leukocyte antigen (HLA)-types presenting BKPyV-encoded immunodominant 9mers. For clinical translation, these data need to be assessed in appropriately designed clinical studies, as outlined in recent guidelines on BKPyV in kidney transplantation. SUMMARY: Evaluation of BKPyV-specific immune responses in recipient and donor may help to stratify the risk of BKPyV-DNAemia, nephropathy, and graft loss. Future efforts need to evaluate clinical translation, vaccines, and immunotherapy to control BKPyV replication.
PURPOSE OF REVIEW: BK polyomavirus (BKPyV) has emerged as a significant cause of premature graft failure after kidney transplantation. Without effective antiviral drugs, treatment is based on reducing immunosuppression to regain immune control over BKPyV replication. The paradigm of high-level viruria/decoy cells, BKPyV-DNAemia, and proven nephropathy permits early interventions. Here, we review recent findings about BKPyV-specific antibody and T-cell responses and their potential role in risk stratification, immune monitoring, and therapy. RECENT FINDING: Kidney transplant recipients having low or undetectable BKPyV-specific IgG immunoglobulin G (IgG) are higher risk for developing BKPyV-DNAemia if the donor has high BKPyV-specific IgG. This observation has been extended to neutralizing antibodies. Immunosuppression, impaired activation, proliferation, and exhaustion of BKPyV-specific T cells may increase the risk of developing BKPyV-DNAemia and nephropathy. Clearance of BKPyV-DNAemia was correlated with high CD8 T cell responses to human leukocyte antigen (HLA)-types presenting BKPyV-encoded immunodominant 9mers. For clinical translation, these data need to be assessed in appropriately designed clinical studies, as outlined in recent guidelines on BKPyV in kidney transplantation. SUMMARY: Evaluation of BKPyV-specific immune responses in recipient and donor may help to stratify the risk of BKPyV-DNAemia, nephropathy, and graft loss. Future efforts need to evaluate clinical translation, vaccines, and immunotherapy to control BKPyV replication.
Authors: Natalia Redondo; Isabel Rodríguez-Goncer; Patricia Parra; Francisco López-Medrano; Esther González; Ana Hernández; Hernando Trujillo; Tamara Ruiz-Merlo; Rafael San Juan; María Dolores Folgueira; Amado Andrés; José María Aguado; Mario Fernández-Ruiz Journal: Sci Rep Date: 2022-07-05 Impact factor: 4.996