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Identification of archetype and rearranged forms of BK virus in leukocytes from healthy individuals
Author(s) -
Chatterjee Malini,
Weyandt Timothy B.,
Frisque Richard J.
Publication year - 2000
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/(sici)1096-9071(200003)60:3<353::aid-jmv16>3.0.co;2-r
Subject(s) - bk virus , virology , biology , t cell receptor , population , virus , serology , titer , archetype , immunology , antibody , medicine , genetics , t cell , immune system , environmental health , kidney transplantation , kidney , art , literature
BK virus (BKV) establishes a persistent, asymptomatic infection in more than 80% of the human population, and in immunocompromised individuals BKV causes acute urinary tract infections. Two forms of BKV, archetype and rearranged, have been recovered previously from urine samples. The rearranged form is believed to have emerged from the archetype form by the deletion and duplication of sequences within the transcriptional control region (TCR). We have PCR‐amplified unique rearranged forms of the BKV TCR from peripheral blood leukocytes (PBLs) of healthy donors. By employing archetype‐specific PCR primers, the archetype BKV TCR was also detected in PBLs. These findings are consistent with the hypotheses that PBLs transport BKV to different sites within the body and play a role in the TCR rearrangement process. BKV sequences were detected in 21 of 38 BKV‐seropositive and 1 of 2 BKV‐seronegative individuals. Because of recent suggestions that SV40 may circulate in the human population, the donors' sera were also examined for the presence of specific anti‐SV40 antibodies. A high antibody titer to SV40 was detected in only 1 of the 40 donor specimens. This study is the first to characterize multiple BKV TCR variants in PBLs from healthy people and to correlate PCR and serological methods used to detect BKV infections. J. Med. Virol. 60:353–362, 2000. © 2000 Wiley‐Liss, Inc.