Hepatitis C virus (HCV) protease variability and anti-HCV protease inhibitor resistance in HIV/HCV-coinfected patients

[Guest guest]

http://onlinelibrary.wiley.com/doi/10.1111/j.1468-1293.2011.00913.x/abstract

Hepatitis C virus (HCV) protease variability and anti-HCV protease inhibitor

resistance in HIV/HCV-coinfected patients

P Trimoulet1,†, C Belzunce2,†, M Faure1, L Wittkop3, S Reigadas1, M Dupon2, J-M

Ragnaud2, H Fleury1, D Neau2

Article first published online: 16 MAR 2011

DOI: 10.1111/j.1468-1293.2011.00913.x

© 2011 British HIV Association

Issue

HIV Medicine

Early View (Articles online in advance of print)

Abstract

Objectives

Data on the natural selection of isolates harbouring mutations within the NS3

protease, conferring resistance to hepatitis C virus (HCV) protease inhibitors

(PIs), are limited for HIV/HCV-coinfected patients. The aim of this study was to

describe the natural prevalence of mutations conferring resistance to HCV PIs in

HIV/HCV-coinfected patients compared with HCV-monoinfected patients.

Methods

The natural prevalences of HCV PI resistance mutations in 120 sequences from

HIV/HCV-coinfected patients (58 genotype 1a, 18 genotype 1b and 44 genotype 4)

and 501 sequences from HCV-monoinfected patients (476 genotype 1 and 25 genotype

4), retrieved from GenBank as a control group, were compared.

Results

Of 76 sequences from HIV/HCV genotype 1-coinfected patients, six (7.9%) showed

amino acid substitutions associated with HCV PI resistance (V36L, n=1; V36M,

n=2; T54S, n=2; R155K, n=1). In 31 of 476 (6.5%) HCV genotype 1 sequences

retrieved from the GenBank database, HCV PI resistance mutations were found. The

difference was not statistically significant (P=0.6). All of the sequences from

HIV/HCV genotype 4-coinfected patients and those retrieved from the GenBank

database had amino acid changes at position 36 (V36L).

Conclusion

Our study suggests that the natural prevalence of strains resistant to HCV PIs

does not differ between HCV-monoinfected and HIV/HCV-coinfected patients.

Further studies on larger cohorts are needed to confirm these findings and to

evaluate the impact of these mutations in clinical practice.

[Guest guest]

http://onlinelibrary.wiley.com/doi/10.1111/j.1468-1293.2011.00913.x/abstract

Hepatitis C virus (HCV) protease variability and anti-HCV protease inhibitor

resistance in HIV/HCV-coinfected patients

P Trimoulet1,†, C Belzunce2,†, M Faure1, L Wittkop3, S Reigadas1, M Dupon2, J-M

Ragnaud2, H Fleury1, D Neau2

Article first published online: 16 MAR 2011

DOI: 10.1111/j.1468-1293.2011.00913.x

© 2011 British HIV Association

Issue

HIV Medicine

Early View (Articles online in advance of print)

Abstract

Objectives

Data on the natural selection of isolates harbouring mutations within the NS3

protease, conferring resistance to hepatitis C virus (HCV) protease inhibitors

(PIs), are limited for HIV/HCV-coinfected patients. The aim of this study was to

describe the natural prevalence of mutations conferring resistance to HCV PIs in

HIV/HCV-coinfected patients compared with HCV-monoinfected patients.

Methods

The natural prevalences of HCV PI resistance mutations in 120 sequences from

HIV/HCV-coinfected patients (58 genotype 1a, 18 genotype 1b and 44 genotype 4)

and 501 sequences from HCV-monoinfected patients (476 genotype 1 and 25 genotype

4), retrieved from GenBank as a control group, were compared.

Results

Of 76 sequences from HIV/HCV genotype 1-coinfected patients, six (7.9%) showed

amino acid substitutions associated with HCV PI resistance (V36L, n=1; V36M,

n=2; T54S, n=2; R155K, n=1). In 31 of 476 (6.5%) HCV genotype 1 sequences

retrieved from the GenBank database, HCV PI resistance mutations were found. The

difference was not statistically significant (P=0.6). All of the sequences from

HIV/HCV genotype 4-coinfected patients and those retrieved from the GenBank

database had amino acid changes at position 36 (V36L).

Conclusion

Our study suggests that the natural prevalence of strains resistant to HCV PIs

does not differ between HCV-monoinfected and HIV/HCV-coinfected patients.

Further studies on larger cohorts are needed to confirm these findings and to

evaluate the impact of these mutations in clinical practice.