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Factors Associated with High HCV Viral Load in HIV/HCV Co-infected Patients: Is There a Different Effect between PI and Non-PI-based ART?
Firouze Bani-Sadr*1, I Goderel1, P Morand2, F Lunel-Fabiani3, C Payan3, P Cacoub4, S Pol5, C Perronne6, F Carrat1, and ANRS HC02 – Ribavic Study team
1Groupe Hosp Univ Est, Univ Paris 6, INSERM U707, France; 2Ctr Hosp Univ Grenoble, France; 3Ctr Hosp Univ Angers, France; 4Groupe Hosp Univ Est, Univ Paris 6, France; 5Groupe Hosp Univ Ouest, Univ Paris 5, INSERM U567, France; and 6Ctr Hosp Univ Raymond Poincare, Univ de Versailles, Garches
Background: Improving our knowledge about the factors
associated with high hepatitis C virus (HCV) viral load may be useful to
optimize the timing and the nature of antiviral therapies in HCV/HIV-co-infected
patients.
Methods: Relationships between HCV viral load and host
factors, viral factors, and HIV treatment in a large population of HIV/HCV-co-infected
patients were analyzed. Baseline variables chosen for statistical analysis were
age, sex, HCV transmission group, mean METAVIR scores for hepatic necroinflammation
and fibrosis, cirrhosis, duration of HCV infection, HCV genotype, duration of
HIV infection, prior AIDS diagnosis, HIV viral load, a HIV viral load below 400
copies/mL, CD4 cell count, ART, mean duration of ART, use of non-nucleoside
reverse transcriptase inhibitors (NNRTI) or protease inhibitors (PI).
Results: A total of 379 patients were included in the
analysis: 312 patients (82.3%) had been receiving
ART for a mean period of 4.37 (3.3) years. The mean baseline CD4 cell count was 528/mm3
(±244), and 65.7% of patients had plasma HIV viral load below <200 copies/mL.
Multiple linear regression analysis identified 2 independent factors associated
with higher HCV viral load: HCV genotype
1 or 4 (b+0.32±0.1, p = 0.0022) and PI-based ART (b+0.28±0.12, p = 0.0247). In contrast, ART was
independently associated with a lower HCV viral load (b–0.31±0.12, p = 0.0128). Thus, the mean HCV RNA level was 6.07±0.71 log10
IU/mL in the 67 patients not receiving ART versus 5.83±0.74 log10 IU/mL (p = 0.0089) in the
312 patients receiving the ART. In contrast, the mean HCV RNA level was 5.96±0.63 log10
IU/mL in the 148 patients with protease inhibitor (PI)- containing regimens versus 5.71±0.8
log10 IU/mL (p = 0.0144) in the 164 patients without PI-containing regimens.
Conclusions: The lower HCV viral load observed in patients
receiving ART without PI compared to both not treated patients and patients
receiving PI-containing ART suggest that firstly, immune reconstitution or a prolonged
period of HIV suppression could lead to the control of HCV replication, and,
secondly, that kinetics of HCV viral load could differ according
HAART-containing regimen.
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