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Seroprevalence of GB virus C and persistence of RNA and antibody

Exposure to GB virus C (GBV‐C) was determined in several U.S. populations by both reverse‐transcription‐polymerase chain reaction (RT‐PCR) and by an enzyme linked immunosorbent assay (ELISA) for antibodies to mammalian cell‐expressed GBV‐C envelope protein, E2 (GBV‐C E2). Most individuals exposed to...

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Published in:Journal of medical virology 1997-10, Vol.53 (2), p.167-173
Main Authors: Gutierrez, Robin A., Dawson, George J., Knigge, Mark F., Melvin, Susan L., Heynen, Cynthia A., Kyrk, Charles R., Young, Charles E., Carrick, Robert J., Schlauder, George G., Surowy, Teresa K., Dille, Bruce J., Coleman, Paul F., Thiele, Dwain L., Lentino, Joseph R., Pachucki, Constance, Mushahwar, Isa K.
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Language:English
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Summary:Exposure to GB virus C (GBV‐C) was determined in several U.S. populations by both reverse‐transcription‐polymerase chain reaction (RT‐PCR) and by an enzyme linked immunosorbent assay (ELISA) for antibodies to mammalian cell‐expressed GBV‐C envelope protein, E2 (GBV‐C E2). Most individuals exposed to GBV‐C were either RNA positive/ELISA negative or ELISA positive/RNA negative. Exposure, therefore, was measured as the sum of GBV‐C RNA positive and GBV‐C E2 antibody positive specimens, and was higher in commercial plasmapheresis donors (40.5%) than in volunteer blood donors (5.5%). In intravenous drug users (IVDUs), GBV‐C exposure was 89.2%. Serial bleed specimens tested for GBV‐C RNA indicate that some patients remain viremic for at least 3 years and fail to produce detectable antibodies to GBV‐C E2. In other exposed individuals who tested negative for GBV‐C RNA, antibodies to E2 appear to be similarly long‐lived (greater than 3 years) with a fairly constant titer (ranging in reciprocal endpoint dilution from 336 to 21,504). Since the detection of GBV‐C RNA and GBV‐C E2 antibody are mutually exclusive in most exposed individuals, studies pertaining to incidence and prevalence of GBV‐C infection require both antibody and nucleic acid detection. J. Med. Virol. 53:167–173, 1997. © 1997 Wiley‐Liss, Inc.
ISSN:0146-6615
1096-9071
DOI:10.1002/(SICI)1096-9071(199710)53:2<167::AID-JMV10>3.0.CO;2-G