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Distinct prevalence of antibodies to the E2 protein of GB virus C/hepatitis G virus in different parts of the world
Author(s) -
Ross R. S.,
Viazov S.,
Schmitt U.,
Schmolke S.,
Tacke M.,
OfenlochHaehnle B.,
Holtmann M.,
Müller N.,
Da Villa G.,
Yoshida C. F.,
Oliveira J. M.,
Szabo A.,
Paladi N.,
Kruppenbacher J. P.,
Philipp Th.,
Roggendorf M.
Publication year - 1998
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(199802)54:2<103::aid-jmv6>3.0.co;2-a
Subject(s) - virology , serology , gb virus c , seroprevalence , hepatitis c virus , virus , flaviviridae , medicine , antibody , hepatitis e virus , viral disease , biology , immunology , genotype , biochemistry , gene
Since the identification of the new human virus, GB virus C (GBV‐C)/hepatitis G virus (HGV), in 1995/1996, reverse transcription polymerase chain reaction remained the sole available diagnostic tool for GBV‐C/HGV infection. Recently, a serologic test based on the detection of antibodies to the putative envelope protein 2 (anti‐E2) has been introduced. We used this assay for a seroepidemiological survey including 3,314 healthy individuals from different parts of the world, 123 patients from Germany who were suspected to have an increased risk of acquiring GBV‐C/HGV infection, 128 multiple organ donors, and 90 GBV‐C/HGV RNA positive persons. In European countries, anti‐E2 seropositivity ranged from 10.9% (Germany) to 15.3% (Austria). In South Africa (20.3%) and Brazil (19.5%), even higher anti‐E2 prevalence rates were recorded. In Asian countries like Bhutan (3.9%), Malaysia (6.3%), and the Philippines (2.7%), anti‐E2 positivity was significantly lower. GBV‐C/HGV anti‐E2 prevalence in potential “risk groups,” i.e., patients on hemodialysis and renal transplant recipients, did not vary significantly from anti‐E2 seroprevalence in German blood donors. Anti‐E2 and GBV‐C/HGV RNA were found to be mutually exclusive, confirming the notion that anti‐E2 has to be considered as a marker of past infection. J. Med. Virol. 54:103–106, 1998. © 1998 Wiley‐Liss,Inc.