Journal
JOURNAL OF CLINICAL VIROLOGY
Volume 42, Issue 2, Pages 198-202Publisher
ELSEVIER
DOI: 10.1016/j.jcv.2008.01.005
Keywords
BK virus; JC virus; large T antigen; cytotoxic T lymphocytes; tetramer; polyomavirus nephropathy; progressive multifocal leukoencephalopathy
Categories
Funding
- NIAID NIH HHS [NS/AI 041198] Funding Source: Medline
- NINDS NIH HHS [K24 NS060950, R01 NS041198-07, K24 NS060950-01, R56 NS041198, R01 NS041198, R01 NS047029-04, R01 NS047029] Funding Source: Medline
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Background: BK 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. Objectives: To 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 design: We 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. Results: CD8(+) T-cells that recognized the nonamer BKV Tp(579), which is identical to JCV Tp(578), 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 Tp(398-) and T-p410-specific CD8(+) T cells were detected in 3/13 (23%) and 1/13 (8%) healthy individuals only. Conclusion: These 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. (c) 2008 Elsevier B.V. All rights reserved.
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