• Yiping Chen, Jennifer Trofe, Jennifer Gordon, Patrick Autissier, E Steve Woodle, and Igor J Koralnik.
• Division of Viral Pathogenesis, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
• J. Clin. Virol. 2008 Jun 1; 42 (2): 198-202.

BackgroundBK virus (BKV), which causes polyomavirus-associated nephropathy (PVN) in kidney transplant recipients (KTx), has 75% homology with JC virus (JCV), the etiologic agent of progressive multifocal leukoencephalopathy (PML). The large T-antigen (T-ag) is the main regulatory protein of polyomaviruses that is expressed early in the viral cycle.ObjectivesTo characterize epitopes of BKV and JCV T-ag recognized by CD8+ T-cells and explore the role of these cells in containing polyomavirus infection.Study DesignWe tested peripheral blood mononuclear cells of HLA A*0201+ BKV- and JCV-seropositive individuals, including patients with active BKV or JCV infection and healthy control subjects in a cross-sectional study.ResultsCD8+ T-cells that recognized the nonamer BKV Tp579, which is identical to JCV Tp578, were detected by tetramer staining in 10/13 (77%) healthy individuals, 3/10 (30%) KTx/PVN, and 4/9 (44%) patients with PML and/or HIV-infection. Conversely, BKV Tp398- and Tp410-specific CD8+ T cells were detected in 3/13 (23%) and 1/13 (8%) healthy individuals only.ConclusionThese data suggest that, as it is the case for the VP1 protein, the same population of CD8+ T-cells may recognize epitopes located on the BKV and JCV T protein. The overall cellular immune response against polyomavirus T-ag, however, is lower than against the VP1 protein and is more frequently detected in healthy individuals than in patients with active BKV or JCV infection.

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