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Amplification of GB virus‐C/hepatitis G virus RNA with primers from different regions of the viral genome
Author(s) -
Kao J. H.,
Chen P. J.,
Chen W.,
Hsiang S. C.,
Lai M. Y.,
Chen D. S.
Publication year - 1997
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(199704)51:4<284::aid-jmv5>3.0.co;2-1
Subject(s) - virology , gb virus c , biology , genome , virus , rna , untranslated region , primer (cosmetics) , microbiology and biotechnology , polymerase chain reaction , flaviviridae , hepatitis c virus , genetics , gene , chemistry , organic chemistry
GB virus‐C/hepatitis G virus (GBV‐C/HGV) is a newly identified RNA virus. The aim of the study was to compare three primer pairs from the 5′ untranslated region (5′UTR), envelope region 2 (E 2) and nonstructural region 3 (NS 3) of GBV‐C/HGV genome for their ability to detect GBV‐C/HGV RNA by polymerase chain reaction (PCR) assays. By using PCR with primers from different regions of the viral genome, serum GBV‐C/HGV RNA was assayed in 200 at‐risk individuals. The sensitivity of this assay was assessed by a titration experiment, and nucleotide sequences of the amplified products were determined directly. Of 200 serum samples, 43 (21.5%) were positive for GBV‐C/HGV RNA with at least one of the primer pairs. The positive rates by 5′UTR, NS 3, and E 2 primers were 100%, 98%, and 84%, respectively, and the sensitivity of PCR assays using 5′UTR primers was 10 to 100 times more likely to detect GBV‐C/HGV RNA than that of NS 3 and E 2 primers. The average homology of amplified targets to the prototype HGV genome was 89%, 80%, and 85% and the similarity between each amplified target was up to 100%, 90%, and 92% in the 5′UTR, E 2, and NS 3 regions, respectively. Therefore, the 5′UTR of GBV‐C/HGV genome is highly conserved and primers deduced from this region can provide a sensitive and specific PCR assay for GBV‐C/HGV RNA. J. Med. Virol. 51:284–289, 1997. © 1997 Wiley‐Liss, Inc.