Abstract
To describe the virological profile of HCV in HBV/HCV co-infection, we investigated the variability of HVR-1 and NS5A domains, which may be involved in viral persistence and replication efficiency. We studied 95 patients: 37 with serological markers of HBV/HCV co-infection, 33 with single HBV and 25 with single HCV infection. HVR-1 complexity and NS5A gene variability were respectively explored by means of PCR-SSCP and direct sequencing. Serum HBV genomes were detected in all coinfected patients: 19 also had circulating HCV particles (group BC-I), whereas HCV were undetectable in the other 18 (group BC-II). Group BC-I was characterised by a significantly lower HBV replication capacity, that reflects the replicative dominance of HCV, although the dominant virus had the same degree of variability as the HCV in single infection. HBV viral load was higher in group BC-II, but not significantly different from that observed in the single infection. Our data indicate an alternation in replicative dominance in co-infection: HBV can suppress HCV replication to undetectable levels, whereas HCV may reduce but does not abrogate the replication capacity of HBV Furthermore, in the cases of HCV dominance, circulating HBV genomes did not have a significant effect on the viral heterogeneity of HCV.
| Original language | English |
|---|---|
| Pages (from-to) | 261-271 |
| Number of pages | 11 |
| Journal | Archives of Virology |
| Volume | 150 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - Feb 2005 |
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ASJC Scopus subject areas
- Genetics
- Applied Microbiology and Biotechnology
Cite this
Genetic variability of hepatitis C virus in HBV/HCV co-infection and HCV single-infection. / De Mitri, M. S.; Morsica, G.; Cassini, R.; Bagaglio, S.; Andreone, P.; Bianchi, G.; Margotti, M.; Bernardi, M.
In: Archives of Virology, Vol. 150, No. 2, 02.2005, p. 261-271.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Genetic variability of hepatitis C virus in HBV/HCV co-infection and HCV single-infection
AU - De Mitri, M. S.
AU - Morsica, G.
AU - Cassini, R.
AU - Bagaglio, S.
AU - Andreone, P.
AU - Bianchi, G.
AU - Margotti, M.
AU - Bernardi, M.
PY - 2005/2
Y1 - 2005/2
N2 - To describe the virological profile of HCV in HBV/HCV co-infection, we investigated the variability of HVR-1 and NS5A domains, which may be involved in viral persistence and replication efficiency. We studied 95 patients: 37 with serological markers of HBV/HCV co-infection, 33 with single HBV and 25 with single HCV infection. HVR-1 complexity and NS5A gene variability were respectively explored by means of PCR-SSCP and direct sequencing. Serum HBV genomes were detected in all coinfected patients: 19 also had circulating HCV particles (group BC-I), whereas HCV were undetectable in the other 18 (group BC-II). Group BC-I was characterised by a significantly lower HBV replication capacity, that reflects the replicative dominance of HCV, although the dominant virus had the same degree of variability as the HCV in single infection. HBV viral load was higher in group BC-II, but not significantly different from that observed in the single infection. Our data indicate an alternation in replicative dominance in co-infection: HBV can suppress HCV replication to undetectable levels, whereas HCV may reduce but does not abrogate the replication capacity of HBV Furthermore, in the cases of HCV dominance, circulating HBV genomes did not have a significant effect on the viral heterogeneity of HCV.
AB - To describe the virological profile of HCV in HBV/HCV co-infection, we investigated the variability of HVR-1 and NS5A domains, which may be involved in viral persistence and replication efficiency. We studied 95 patients: 37 with serological markers of HBV/HCV co-infection, 33 with single HBV and 25 with single HCV infection. HVR-1 complexity and NS5A gene variability were respectively explored by means of PCR-SSCP and direct sequencing. Serum HBV genomes were detected in all coinfected patients: 19 also had circulating HCV particles (group BC-I), whereas HCV were undetectable in the other 18 (group BC-II). Group BC-I was characterised by a significantly lower HBV replication capacity, that reflects the replicative dominance of HCV, although the dominant virus had the same degree of variability as the HCV in single infection. HBV viral load was higher in group BC-II, but not significantly different from that observed in the single infection. Our data indicate an alternation in replicative dominance in co-infection: HBV can suppress HCV replication to undetectable levels, whereas HCV may reduce but does not abrogate the replication capacity of HBV Furthermore, in the cases of HCV dominance, circulating HBV genomes did not have a significant effect on the viral heterogeneity of HCV.
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UR - http://www.scopus.com/inward/citedby.url?scp=12944273356&partnerID=8YFLogxK
U2 - 10.1007/s00705-004-0415-7
DO - 10.1007/s00705-004-0415-7
M3 - Article
VL - 150
SP - 261
EP - 271
JO - Archives of Virology
JF - Archives of Virology
SN - 0304-8608
IS - 2
ER -