QUANTITATION OF HEPATITIS-G AND HEPATITIS-C VIRUSES IN THE LIVER - EVIDENCE THAT HEPATITIS-G VIRUS IS NOT HEPATOTROPIC

Citation
Mg. Pessoa et al., QUANTITATION OF HEPATITIS-G AND HEPATITIS-C VIRUSES IN THE LIVER - EVIDENCE THAT HEPATITIS-G VIRUS IS NOT HEPATOTROPIC, Hepatology, 27(3), 1998, pp. 877-880
Citations number
19
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
02709139
Volume
27
Issue
3
Year of publication
1998
Pages
877 - 880
Database
ISI
SICI code
0270-9139(1998)27:3<877:QOHAHV>2.0.ZU;2-8
Abstract
Hepatitis G virus (HGV) is prevalent in patients with chronic liver di sease and has been previously detected in liver specimens. However, it is unknown whether the virus is replicating in the liver or is simply a contaminant from serum. We sought to determine whether HGV was hepa totropic and to determine whether coinfection with HGV and hepatitis C virus (HCV) influenced the level of either virus. Virus was quantitat ed using branched DNA (bDNA) assay for both HGV and HCV in the liver e xplants and pretransplant serum samples from 30 transplant recipients: Group I, HGV/HCV coinfection (n = 10); group II, HCV infection alone, (n = 8); group III, HGV alone (n = 12). In patients with coinfection HCV (RNA) titers in liver were consistently higher than those for HGV RNA (median 1.13 x 10(8) and 360,000 Eq/g respectively, P < .01). The ratio of liver/serum viral RNA was significantly higher for HCV than f or HGV (median 129 and 0.3 respectively, P < .01). Levels of HCV RNA w ere similar in patients with HCV infection alone versus those with HGV /HCV coinfection (median; liver = 1.15 x 10(7) vs. 1.13 x 10(8) Eq/g, serum = 500,000 vs. 200,000 Eq/mL) and levels of HGV RNA in liver and serum were similar in patients with HGV infection alone compared to th ose with HGV/HCV coinfection (median; liver = 1.2 x 10(6) vs. 4.0 x 10 (5) Eq/g, serum = 4.5 x 10(6) vs. 2.6 x 10(6) Eq/mL), Levels of either virus appeared unaffected by the presence of an additional virus, The high ratio of HCV RNA levels in liver compared to serum is consistent with its known hepatotropism, but this pattern was not observed for H GV. The median liver/serum ratio of HGV RNA was less than unity, a fin ding consistent with serum contamination of liver tissue, Thus we conc lude that the liver is not the main site of HGV replication.