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Session 106 Poster Presentations
GBV-C and SENV: Good, Bad, or Indifferent?
Session Day and Time: Wednesday 1:30 - 3:30 pm
Room: Hall B


849
Slower Disease Progression and Greater CD4 Response to Antiretroviral Treatment in HIV Patients Co-infected with GBV-C
J. P. Aboulker*1, V. Chams-Harvey2, P. Flandre1, S. Delarue2, S. Leonardo1, P. Yeni2, D. Descamps2, F. Brun-Vézinet2
1INSERM SC10, Villejuif, France and 2Hosp Bichat-Claude Bernard, Paris, France

Background : Although most studies so far have consistently reported higher CD4 cell counts and lower HIV RNA in untreated HIV-infected patients (pts) co-infected with GBV-C, whether and how GBV-C impacts on HIV disease progression (DP) remains uncertain. To control for Antiretroviral Treatment (ART) received, we studied GBV-C co-infection in a 3-yr randomized trial with clinical end-points.
Methods: A cohort of 326 untreated pts randomized to AZT alone or in combination with DDI or DDC was sampled from Delta (1992-1995). The presence of GBV-C was determined at baseline (BL) by 2 rounds of RT-PCR (Titan One Tube, Roche Diagnostics) on RNA extracted from serum. CD4, HIV RNA (Nasba technic) and clinical events were recorded every 2-4 months. GBV-C positive and negative pts were compared both at BL and longitudinally using Cox models including BL variables either alone or combined to the CD4 response.
Results: The cohort population was similar to the whole Delta trial population in respect to BL characteristics. Ninety-seven (97) out of 326 (29.8%, CI95 24.8-34.7) were GBV-C RNA positive. Prevalence was similar across risk groups. GBV-C positive pts were younger (mean: 34 vs 37 yrs) had significantly higher CD4 cell counts (252 vs 224/ml) and lower HIV RNA (4.56 vs 4.72) than negative pts. GBV-C positive and negative pts were equally distributed across the 3 treatment arms. During a 29 mos median follow-up, 79 pts progressed either to AIDS (n = 40) or death (n = 39). Adjusted on BL CD4, BL HIV RNA and sex, DP was slower (OR = 0.45, CI95, 0.2-0.9) in GBV-C positive compared to negative pts. Reduction in HIV RNA was identical in GBV-C positive and negative pts. In contrast, increase in CD4 cell count was greater in positive than in negative pts in particular at W64 (p = 0.05), and W80 (p = 0.04) with a trend toward slower return to BL value (p = 0.07). When adjusted on CD4 response, in addition to BL characteristics, DP was no longer significantly different in positive and negative pts.
Conclusion: In this cohort, GBV-C co-infected pts had a better CD4 response to ART than GBV-C negative pts which explained in part their slower progression to AIDS or death. Immunologic implications of GBV-C co-infection in HIV should be further investigated.