1039
Longitudinal Evaluation of Hepatitis B, C, or D Viremia in HIV-HBV-co-infected Patients: Virological Interactions and Effects of Treatment
Anders Boyd*1, K Lacombe1,2,3, P Miailhes4, J Gozlan2,3, P Bonnard5, J M Molina6, C Lascoux-Combe6, L Serfaty3, M Desvarieux1,2,7, and P M Girard2,3
1INSERM UMR S707, Paris, France; 2Univ Pierre and Marie Curie, Paris, France; 3Hosp St Antoine, Paris, France; 4Hosp Hotel Dieu, Hosp Civils de Lyon, France; 5Hosp Tenon, Paris, France; 6Hosp St Louis, Paris, France; and 7Columbia Univ Mailman Sch of Publ Hlth, New York, NY, US
Background: In the context of HIV-infected patients,
virological interactions of hepatitis B (HBV), hepatitis C (HCV), and hepatitis
D (HDV) viruses have been poorly characterized and treatment influences have
not been analyzed.
Methods: Viral fluctuations were prospectively
studied during a 3-year period in a cohort of 308 HIV/HBV-co-infected patients.
Undetectability rates of HBV DNA, HCV RNA, and HDV RNA were summarized and compared
using GEE models with calculation of OR adjusted for serum HIV RNA, CD4 cell
count, concurrent treatment with lamivudine and tenofovir, and concurrent or
prior treatment with peg-interferon. Influence of treatment was separately evaluated
by the changes of viral detection in the presence of treatment.
Results: Hepatic co-infection in HIV-infected patients
(age in years, SD) was as follows: 266 HBV (40.7, 8.2); 18 HBV/HCV (39.7, 4.2);
15 HBV/HDV (36.0, 9.0); and 9 HBV/HCV/HDV (39.1, 6.1). Lamivudine and tenofovir
were taken in 87.0% and 17.5% of patients respectively and did not differ
across co-infection groups (p = 0.2, p = 0.7). HDV co-infected
patients used interferon therapy more frequently (p = 0.02). Hepatitis B
virus suppression was significantly associated with the presence of HDV
co-infection (aOR = 9.85, 95%CI 3.49 to 24.86, p <0.001), whereas
only marginal or lacking suppression was found in the presence of HCV and
HCV/HDV co-infection (aOR = 2.31, 95%CI 0.89 to –5.96, p = 0.08 and aOR =
1.42, 95%CI 0.50 to 4.00, p = 0.5 respectively). HBV/HCV/HDV infection
was associated with a modest suppression of HCV replication (p = 0.06)
and no difference in HDV replication (p = 0.8). HIV-replication was
associated with diminished HBV replication (p <0.001), an effect not observed
on HCV or HDV replication. Tenofovir had a more suppressive effect on HBV
replication (aOR = 3.64, 95%CI 2.57 to 5.16, p <0.001) while
peg-interferon had a minor effect on HCV (p = 0.08) and HDV (p = 0.06)
replication. HDV-replication was more uncontrolled by treatment than HCV (p =
0.04).
Conclusions: In comparing detection among hepatic
virus, it appears that HDV exerts a dominate impact on HBV and HCV replication,
even under the influence of treatment, CD4 cell count and HIV replication.
Future studies must consider the viral detectability under the influence of
treatment, which can only be assessed in longitudinal evaluation.
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